| CANX and EBI3 |
calnexin |
Epstein-Barr virus induced 3 |
- Diseases of glycosylation
- Defective ALG14 causes congenital myasthenic syndrome (ALG14-CMS)
- Defective MGAT2 causes MGAT2-CDG (CDG-2a)
- Defective ALG1 causes ALG1-CDG (CDG-1k)
- Antigen Presentation: Folding, assembly and peptide loading of class I MHC
- Virus Assembly and Release
- Defective MOGS causes MOGS-CDG (CDG-2b)
- Influenza Life Cycle
- Defective ALG9 causes ALG9-CDG (CDG-1l)
- Defective MAN1B1 causes MRT15
- MHC class II antigen presentation
- Class I MHC mediated antigen processing & presentation
- N-glycan trimming in the ER and Calnexin/Calreticulin cycle
- Assembly of Viral Components at the Budding Site
- Defective ALG11 causes ALG11-CDG (CDG-1p)
- Defective ALG2 causes ALG2-CDG (CDG-1i)
- Post-translational protein modification
- Defective ALG3 causes ALG3-CDG (CDG-1d)
- Defective DPAGT1 causes DPAGT1-CDG (CDG-1j) and CMSTA2
- Defective B4GALT1 causes B4GALT1-CDG (CDG-2d)
- Influenza Infection
- Defective RFT1 causes RFT1-CDG (CDG-1n)
- Defective ALG6 causes ALG6-CDG (CDG-1c)
- Asparagine N-linked glycosylation
- Defective ALG8 causes ALG8-CDG (CDG-1h)
- Defective MPDU1 causes MPDU1-CDG (CDG-1f)
- Defective ALG12 causes ALG12-CDG (CDG-1g)
- Diseases associated with N-glycosylation of proteins
- Adaptive Immune System
- Calnexin/calreticulin cycle
|
|
- Antihemophilic Factor
- Tenecteplase
|
|
|
|
| CANX and CSNK2A1 |
calnexin |
casein kinase 2, alpha 1 polypeptide |
- Diseases of glycosylation
- Defective ALG14 causes congenital myasthenic syndrome (ALG14-CMS)
- Defective MGAT2 causes MGAT2-CDG (CDG-2a)
- Defective ALG1 causes ALG1-CDG (CDG-1k)
- Antigen Presentation: Folding, assembly and peptide loading of class I MHC
- Virus Assembly and Release
- Defective MOGS causes MOGS-CDG (CDG-2b)
- Influenza Life Cycle
- Defective ALG9 causes ALG9-CDG (CDG-1l)
- Defective MAN1B1 causes MRT15
- MHC class II antigen presentation
- Class I MHC mediated antigen processing & presentation
- N-glycan trimming in the ER and Calnexin/Calreticulin cycle
- Assembly of Viral Components at the Budding Site
- Defective ALG11 causes ALG11-CDG (CDG-1p)
- Defective ALG2 causes ALG2-CDG (CDG-1i)
- Post-translational protein modification
- Defective ALG3 causes ALG3-CDG (CDG-1d)
- Defective DPAGT1 causes DPAGT1-CDG (CDG-1j) and CMSTA2
- Defective B4GALT1 causes B4GALT1-CDG (CDG-2d)
- Influenza Infection
- Defective RFT1 causes RFT1-CDG (CDG-1n)
- Defective ALG6 causes ALG6-CDG (CDG-1c)
- Asparagine N-linked glycosylation
- Defective ALG8 causes ALG8-CDG (CDG-1h)
- Defective MPDU1 causes MPDU1-CDG (CDG-1f)
- Defective ALG12 causes ALG12-CDG (CDG-1g)
- Diseases associated with N-glycosylation of proteins
- Adaptive Immune System
- Calnexin/calreticulin cycle
|
- Mitotic Prometaphase
- Signal transduction by L1
- Axon guidance
- misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling
- L1CAM interactions
- Signaling by Wnt
- Cell Cycle, Mitotic
- M Phase
- WNT mediated activation of DVL
- TCF dependent signaling in response to WNT
- RNF mutants show enhanced WNT signaling and proliferation
- XAV939 inhibits tankyrase, stabilizing AXIN
- Signaling by WNT in cancer
- Condensation of Prometaphase Chromosomes
|
- Antihemophilic Factor
- Tenecteplase
|
- (5-Oxo-5,6-Dihydro-Indolo[1,2-a]Quinazolin-7-Yl)-Acetic Acid
- 1,8-Di-Hydroxy-4-Nitro-Xanthen-9-One
- Resveratrol
- 1,8-Di-Hydroxy-4-Nitro-Anthraquinone
- Benzamidine
- 5,8-Di-Amino-1,4-Dihydroxy-Anthraquinone
- Phosphoaminophosphonic Acid-Adenylate Ester
- Tetrabromo-2-Benzotriazole
- DIMETHYL-(4,5,6,7-TETRABROMO-1H-BENZOIMIDAZOL-2-YL)-AMINE
- S-METHYL-4,5,6,7-TETRABROMO-BENZIMIDAZOLE
- N1,N2-ETHYLENE-2-METHYLAMINO-4,5,6,7-TETRABROMO-BENZIMIDAZOLE
- 3-METHYL-1,6,8-TRIHYDROXYANTHRAQUINONE
- 3,8-DIBROMO-7-HYDROXY-4-METHYL-2H-CHROMEN-2-ONE
- 19-(cyclopropylamino)-4,6,7,15-tetrahydro-5H-16,1-(azenometheno)-10,14-(metheno)pyrazolo[4,3-o][1,3,9]triazacyclohexadecin-8(9H)-one
- N,N\'-DIPHENYLPYRAZOLO[1,5-A][1,3,5]TRIAZINE-2,4-DIAMINE
- 4-(2-(1H-IMIDAZOL-4-YL)ETHYLAMINO)-2-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(CYCLOHEXYLMETHYLAMINO)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(4-CHLOROBENZYLAMINO)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- 2-(4-ETHYLPIPERAZIN-1-YL)-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZINE-8-CARBONITRILE
- N-(3-(8-CYANO-4-(PHENYLAMINO)PYRAZOLO[1,5-A][1,3,5]TRIAZIN-2-YLAMINO)PHENYL)ACETAMIDE
- 2,3,7,8-tetrahydroxychromeno[5,4,3-cde]chromene-5,10-dione
- 5,6-dichloro-1-beta-D-ribofuranosyl-1H-benzimidazole
- 1,2,5,8-tetrahydroxyanthracene-9,10-dione
- Ellagic Acid
|
|
|
| CANX and LPA |
calnexin |
lipoprotein, Lp(a) |
- Diseases of glycosylation
- Defective ALG14 causes congenital myasthenic syndrome (ALG14-CMS)
- Defective MGAT2 causes MGAT2-CDG (CDG-2a)
- Defective ALG1 causes ALG1-CDG (CDG-1k)
- Antigen Presentation: Folding, assembly and peptide loading of class I MHC
- Virus Assembly and Release
- Defective MOGS causes MOGS-CDG (CDG-2b)
- Influenza Life Cycle
- Defective ALG9 causes ALG9-CDG (CDG-1l)
- Defective MAN1B1 causes MRT15
- MHC class II antigen presentation
- Class I MHC mediated antigen processing & presentation
- N-glycan trimming in the ER and Calnexin/Calreticulin cycle
- Assembly of Viral Components at the Budding Site
- Defective ALG11 causes ALG11-CDG (CDG-1p)
- Defective ALG2 causes ALG2-CDG (CDG-1i)
- Post-translational protein modification
- Defective ALG3 causes ALG3-CDG (CDG-1d)
- Defective DPAGT1 causes DPAGT1-CDG (CDG-1j) and CMSTA2
- Defective B4GALT1 causes B4GALT1-CDG (CDG-2d)
- Influenza Infection
- Defective RFT1 causes RFT1-CDG (CDG-1n)
- Defective ALG6 causes ALG6-CDG (CDG-1c)
- Asparagine N-linked glycosylation
- Defective ALG8 causes ALG8-CDG (CDG-1h)
- Defective MPDU1 causes MPDU1-CDG (CDG-1f)
- Defective ALG12 causes ALG12-CDG (CDG-1g)
- Diseases associated with N-glycosylation of proteins
- Adaptive Immune System
- Calnexin/calreticulin cycle
|
|
- Antihemophilic Factor
- Tenecteplase
|
|
|
|
| CANX and FSHR |
calnexin |
follicle stimulating hormone receptor |
- Diseases of glycosylation
- Defective ALG14 causes congenital myasthenic syndrome (ALG14-CMS)
- Defective MGAT2 causes MGAT2-CDG (CDG-2a)
- Defective ALG1 causes ALG1-CDG (CDG-1k)
- Antigen Presentation: Folding, assembly and peptide loading of class I MHC
- Virus Assembly and Release
- Defective MOGS causes MOGS-CDG (CDG-2b)
- Influenza Life Cycle
- Defective ALG9 causes ALG9-CDG (CDG-1l)
- Defective MAN1B1 causes MRT15
- MHC class II antigen presentation
- Class I MHC mediated antigen processing & presentation
- N-glycan trimming in the ER and Calnexin/Calreticulin cycle
- Assembly of Viral Components at the Budding Site
- Defective ALG11 causes ALG11-CDG (CDG-1p)
- Defective ALG2 causes ALG2-CDG (CDG-1i)
- Post-translational protein modification
- Defective ALG3 causes ALG3-CDG (CDG-1d)
- Defective DPAGT1 causes DPAGT1-CDG (CDG-1j) and CMSTA2
- Defective B4GALT1 causes B4GALT1-CDG (CDG-2d)
- Influenza Infection
- Defective RFT1 causes RFT1-CDG (CDG-1n)
- Defective ALG6 causes ALG6-CDG (CDG-1c)
- Asparagine N-linked glycosylation
- Defective ALG8 causes ALG8-CDG (CDG-1h)
- Defective MPDU1 causes MPDU1-CDG (CDG-1f)
- Defective ALG12 causes ALG12-CDG (CDG-1g)
- Diseases associated with N-glycosylation of proteins
- Adaptive Immune System
- Calnexin/calreticulin cycle
|
- Defective ACTH causes Obesity and Pro-opiomelanocortinin deficiency (POMCD)
- Signaling by GPCR
- GPCR downstream signaling
- G alpha (s) signalling events
- Class A/1 (Rhodopsin-like receptors)
- Hormone ligand-binding receptors
- Metabolic disorders of biological oxidation enzymes
- GPCR ligand binding
|
- Antihemophilic Factor
- Tenecteplase
|
- Menotropins
- Follitropin beta
- Urofollitropin
- Choriogonadotropin alfa
- Suramin
|
|
|
| CANX and MTNR1A |
calnexin |
melatonin receptor 1A |
- Diseases of glycosylation
- Defective ALG14 causes congenital myasthenic syndrome (ALG14-CMS)
- Defective MGAT2 causes MGAT2-CDG (CDG-2a)
- Defective ALG1 causes ALG1-CDG (CDG-1k)
- Antigen Presentation: Folding, assembly and peptide loading of class I MHC
- Virus Assembly and Release
- Defective MOGS causes MOGS-CDG (CDG-2b)
- Influenza Life Cycle
- Defective ALG9 causes ALG9-CDG (CDG-1l)
- Defective MAN1B1 causes MRT15
- MHC class II antigen presentation
- Class I MHC mediated antigen processing & presentation
- N-glycan trimming in the ER and Calnexin/Calreticulin cycle
- Assembly of Viral Components at the Budding Site
- Defective ALG11 causes ALG11-CDG (CDG-1p)
- Defective ALG2 causes ALG2-CDG (CDG-1i)
- Post-translational protein modification
- Defective ALG3 causes ALG3-CDG (CDG-1d)
- Defective DPAGT1 causes DPAGT1-CDG (CDG-1j) and CMSTA2
- Defective B4GALT1 causes B4GALT1-CDG (CDG-2d)
- Influenza Infection
- Defective RFT1 causes RFT1-CDG (CDG-1n)
- Defective ALG6 causes ALG6-CDG (CDG-1c)
- Asparagine N-linked glycosylation
- Defective ALG8 causes ALG8-CDG (CDG-1h)
- Defective MPDU1 causes MPDU1-CDG (CDG-1f)
- Defective ALG12 causes ALG12-CDG (CDG-1g)
- Diseases associated with N-glycosylation of proteins
- Adaptive Immune System
- Calnexin/calreticulin cycle
|
- Defective ACTH causes Obesity and Pro-opiomelanocortinin deficiency (POMCD)
- Signaling by GPCR
- GPCR downstream signaling
- Class A/1 (Rhodopsin-like receptors)
- G alpha (i) signalling events
- Metabolic disorders of biological oxidation enzymes
- GPCR ligand binding
|
- Antihemophilic Factor
- Tenecteplase
|
- Ramelteon
- Melatonin
- Agomelatine
|
|
|
| CANX and MTNR1B |
calnexin |
melatonin receptor 1B |
- Diseases of glycosylation
- Defective ALG14 causes congenital myasthenic syndrome (ALG14-CMS)
- Defective MGAT2 causes MGAT2-CDG (CDG-2a)
- Defective ALG1 causes ALG1-CDG (CDG-1k)
- Antigen Presentation: Folding, assembly and peptide loading of class I MHC
- Virus Assembly and Release
- Defective MOGS causes MOGS-CDG (CDG-2b)
- Influenza Life Cycle
- Defective ALG9 causes ALG9-CDG (CDG-1l)
- Defective MAN1B1 causes MRT15
- MHC class II antigen presentation
- Class I MHC mediated antigen processing & presentation
- N-glycan trimming in the ER and Calnexin/Calreticulin cycle
- Assembly of Viral Components at the Budding Site
- Defective ALG11 causes ALG11-CDG (CDG-1p)
- Defective ALG2 causes ALG2-CDG (CDG-1i)
- Post-translational protein modification
- Defective ALG3 causes ALG3-CDG (CDG-1d)
- Defective DPAGT1 causes DPAGT1-CDG (CDG-1j) and CMSTA2
- Defective B4GALT1 causes B4GALT1-CDG (CDG-2d)
- Influenza Infection
- Defective RFT1 causes RFT1-CDG (CDG-1n)
- Defective ALG6 causes ALG6-CDG (CDG-1c)
- Asparagine N-linked glycosylation
- Defective ALG8 causes ALG8-CDG (CDG-1h)
- Defective MPDU1 causes MPDU1-CDG (CDG-1f)
- Defective ALG12 causes ALG12-CDG (CDG-1g)
- Diseases associated with N-glycosylation of proteins
- Adaptive Immune System
- Calnexin/calreticulin cycle
|
- Defective ACTH causes Obesity and Pro-opiomelanocortinin deficiency (POMCD)
- Signaling by GPCR
- GPCR downstream signaling
- Class A/1 (Rhodopsin-like receptors)
- G alpha (i) signalling events
- Metabolic disorders of biological oxidation enzymes
- GPCR ligand binding
|
- Antihemophilic Factor
- Tenecteplase
|
- Ramelteon
- Melatonin
- Agomelatine
|
|
|
| CANX and LRP1 |
calnexin |
low density lipoprotein receptor-related protein 1 |
- Diseases of glycosylation
- Defective ALG14 causes congenital myasthenic syndrome (ALG14-CMS)
- Defective MGAT2 causes MGAT2-CDG (CDG-2a)
- Defective ALG1 causes ALG1-CDG (CDG-1k)
- Antigen Presentation: Folding, assembly and peptide loading of class I MHC
- Virus Assembly and Release
- Defective MOGS causes MOGS-CDG (CDG-2b)
- Influenza Life Cycle
- Defective ALG9 causes ALG9-CDG (CDG-1l)
- Defective MAN1B1 causes MRT15
- MHC class II antigen presentation
- Class I MHC mediated antigen processing & presentation
- N-glycan trimming in the ER and Calnexin/Calreticulin cycle
- Assembly of Viral Components at the Budding Site
- Defective ALG11 causes ALG11-CDG (CDG-1p)
- Defective ALG2 causes ALG2-CDG (CDG-1i)
- Post-translational protein modification
- Defective ALG3 causes ALG3-CDG (CDG-1d)
- Defective DPAGT1 causes DPAGT1-CDG (CDG-1j) and CMSTA2
- Defective B4GALT1 causes B4GALT1-CDG (CDG-2d)
- Influenza Infection
- Defective RFT1 causes RFT1-CDG (CDG-1n)
- Defective ALG6 causes ALG6-CDG (CDG-1c)
- Asparagine N-linked glycosylation
- Defective ALG8 causes ALG8-CDG (CDG-1h)
- Defective MPDU1 causes MPDU1-CDG (CDG-1f)
- Defective ALG12 causes ALG12-CDG (CDG-1g)
- Diseases associated with N-glycosylation of proteins
- Adaptive Immune System
- Calnexin/calreticulin cycle
|
- Scavenging of heme from plasma
- Visual phototransduction
- Diseases associated with visual transduction
- Retinoid metabolism and transport
|
- Antihemophilic Factor
- Tenecteplase
|
|
|
|
| CANX and PRKCSH |
calnexin |
protein kinase C substrate 80K-H |
- Diseases of glycosylation
- Defective ALG14 causes congenital myasthenic syndrome (ALG14-CMS)
- Defective MGAT2 causes MGAT2-CDG (CDG-2a)
- Defective ALG1 causes ALG1-CDG (CDG-1k)
- Antigen Presentation: Folding, assembly and peptide loading of class I MHC
- Virus Assembly and Release
- Defective MOGS causes MOGS-CDG (CDG-2b)
- Influenza Life Cycle
- Defective ALG9 causes ALG9-CDG (CDG-1l)
- Defective MAN1B1 causes MRT15
- MHC class II antigen presentation
- Class I MHC mediated antigen processing & presentation
- N-glycan trimming in the ER and Calnexin/Calreticulin cycle
- Assembly of Viral Components at the Budding Site
- Defective ALG11 causes ALG11-CDG (CDG-1p)
- Defective ALG2 causes ALG2-CDG (CDG-1i)
- Post-translational protein modification
- Defective ALG3 causes ALG3-CDG (CDG-1d)
- Defective DPAGT1 causes DPAGT1-CDG (CDG-1j) and CMSTA2
- Defective B4GALT1 causes B4GALT1-CDG (CDG-2d)
- Influenza Infection
- Defective RFT1 causes RFT1-CDG (CDG-1n)
- Defective ALG6 causes ALG6-CDG (CDG-1c)
- Asparagine N-linked glycosylation
- Defective ALG8 causes ALG8-CDG (CDG-1h)
- Defective MPDU1 causes MPDU1-CDG (CDG-1f)
- Defective ALG12 causes ALG12-CDG (CDG-1g)
- Diseases associated with N-glycosylation of proteins
- Adaptive Immune System
- Calnexin/calreticulin cycle
|
- Diseases of glycosylation
- Defective ALG14 causes congenital myasthenic syndrome (ALG14-CMS)
- Defective MGAT2 causes MGAT2-CDG (CDG-2a)
- Defective ALG1 causes ALG1-CDG (CDG-1k)
- Defective MOGS causes MOGS-CDG (CDG-2b)
- Defective ALG9 causes ALG9-CDG (CDG-1l)
- Defective MAN1B1 causes MRT15
- N-glycan trimming in the ER and Calnexin/Calreticulin cycle
- Advanced glycosylation endproduct receptor signaling
- Defective ALG11 causes ALG11-CDG (CDG-1p)
- Innate Immune System
- Defective ALG2 causes ALG2-CDG (CDG-1i)
- Post-translational protein modification
- Defective ALG3 causes ALG3-CDG (CDG-1d)
- Defective DPAGT1 causes DPAGT1-CDG (CDG-1j) and CMSTA2
- Defective B4GALT1 causes B4GALT1-CDG (CDG-2d)
- Defective RFT1 causes RFT1-CDG (CDG-1n)
- Defective ALG6 causes ALG6-CDG (CDG-1c)
- Asparagine N-linked glycosylation
- Defective ALG8 causes ALG8-CDG (CDG-1h)
- Defective MPDU1 causes MPDU1-CDG (CDG-1f)
- Defective ALG12 causes ALG12-CDG (CDG-1g)
- Diseases associated with N-glycosylation of proteins
- Calnexin/calreticulin cycle
|
- Antihemophilic Factor
- Tenecteplase
|
|
|
|
| CANX and EDEM1 |
calnexin |
ER degradation enhancer, mannosidase alpha-like 1 |
- Diseases of glycosylation
- Defective ALG14 causes congenital myasthenic syndrome (ALG14-CMS)
- Defective MGAT2 causes MGAT2-CDG (CDG-2a)
- Defective ALG1 causes ALG1-CDG (CDG-1k)
- Antigen Presentation: Folding, assembly and peptide loading of class I MHC
- Virus Assembly and Release
- Defective MOGS causes MOGS-CDG (CDG-2b)
- Influenza Life Cycle
- Defective ALG9 causes ALG9-CDG (CDG-1l)
- Defective MAN1B1 causes MRT15
- MHC class II antigen presentation
- Class I MHC mediated antigen processing & presentation
- N-glycan trimming in the ER and Calnexin/Calreticulin cycle
- Assembly of Viral Components at the Budding Site
- Defective ALG11 causes ALG11-CDG (CDG-1p)
- Defective ALG2 causes ALG2-CDG (CDG-1i)
- Post-translational protein modification
- Defective ALG3 causes ALG3-CDG (CDG-1d)
- Defective DPAGT1 causes DPAGT1-CDG (CDG-1j) and CMSTA2
- Defective B4GALT1 causes B4GALT1-CDG (CDG-2d)
- Influenza Infection
- Defective RFT1 causes RFT1-CDG (CDG-1n)
- Defective ALG6 causes ALG6-CDG (CDG-1c)
- Asparagine N-linked glycosylation
- Defective ALG8 causes ALG8-CDG (CDG-1h)
- Defective MPDU1 causes MPDU1-CDG (CDG-1f)
- Defective ALG12 causes ALG12-CDG (CDG-1g)
- Diseases associated with N-glycosylation of proteins
- Adaptive Immune System
- Calnexin/calreticulin cycle
|
- Diseases of glycosylation
- Defective ALG14 causes congenital myasthenic syndrome (ALG14-CMS)
- Defective MGAT2 causes MGAT2-CDG (CDG-2a)
- Defective ALG1 causes ALG1-CDG (CDG-1k)
- XBP1(S) activates chaperone genes
- Defective MOGS causes MOGS-CDG (CDG-2b)
- IRE1alpha activates chaperones
- Defective ALG9 causes ALG9-CDG (CDG-1l)
- Defective MAN1B1 causes MRT15
- N-glycan trimming in the ER and Calnexin/Calreticulin cycle
- Unfolded Protein Response (UPR)
- Defective ALG11 causes ALG11-CDG (CDG-1p)
- Defective ALG2 causes ALG2-CDG (CDG-1i)
- Defective ALG3 causes ALG3-CDG (CDG-1d)
- Post-translational protein modification
- Defective DPAGT1 causes DPAGT1-CDG (CDG-1j) and CMSTA2
- Defective B4GALT1 causes B4GALT1-CDG (CDG-2d)
- Defective RFT1 causes RFT1-CDG (CDG-1n)
- Defective ALG6 causes ALG6-CDG (CDG-1c)
- Asparagine N-linked glycosylation
- Defective ALG8 causes ALG8-CDG (CDG-1h)
- Defective MPDU1 causes MPDU1-CDG (CDG-1f)
- Defective ALG12 causes ALG12-CDG (CDG-1g)
- ER Quality Control Compartment (ERQC)
- Diseases associated with N-glycosylation of proteins
- Calnexin/calreticulin cycle
|
- Antihemophilic Factor
- Tenecteplase
|
|
|
|
| CASP2 and RPL30 |
caspase 2, apoptosis-related cysteine peptidase |
ribosomal protein L30 |
- Signalling by NGF
- Cell death signalling via NRAGE, NRIF and NADE
- Nucleotide-binding domain, leucine rich repeat containing receptor (NLR) signaling pathways
- NOD1/2 Signaling Pathway
- p75 NTR receptor-mediated signalling
- NADE modulates death signalling
- Innate Immune System
|
- Nonsense-Mediated Decay (NMD)
- Translation
- SRP-dependent cotranslational protein targeting to membrane
- Eukaryotic Translation Termination
- Peptide chain elongation
- Influenza Infection
- Viral mRNA Translation
- L13a-mediated translational silencing of Ceruloplasmin expression
- Influenza Life Cycle
- Nonsense Mediated Decay (NMD) enhanced by the Exon Junction Complex (EJC)
- Influenza Viral RNA Transcription and Replication
- GTP hydrolysis and joining of the 60S ribosomal subunit
- Eukaryotic Translation Initiation
- Formation of a pool of free 40S subunits
- Eukaryotic Translation Elongation
- Cap-dependent Translation Initiation
- Nonsense Mediated Decay (NMD) independent of the Exon Junction Complex (EJC)
|
|
|
|
|
| CASP3 and EIF2AK2 |
caspase 3, apoptosis-related cysteine peptidase |
eukaryotic translation initiation factor 2-alpha kinase 2 |
- SMAC binds to IAPs
- SMAC-mediated dissociation of IAP:caspase complexes
- SMAC-mediated apoptotic response
- Cytochrome c-mediated apoptotic response
- Caspase-mediated cleavage of cytoskeletal proteins
- Degradation of the extracellular matrix
- Role of DCC in regulating apoptosis
- Activation of caspases through apoptosome-mediated cleavage
- Activation of DNA fragmentation factor
- Apoptotic factor-mediated response
- Programmed Cell Death
- Intrinsic Pathway for Apoptosis
- Signalling by NGF
- Apoptotic cleavage of cellular proteins
- Cell death signalling via NRAGE, NRIF and NADE
- Apoptotic execution phase
- p75 NTR receptor-mediated signalling
- Stimulation of the cell death response by PAK-2p34
- Apoptotic cleavage of cell adhesion proteins
- Signaling by Hippo
- Apoptosis induced DNA fragmentation
- Extrinsic Pathway
- NADE modulates death signalling
|
- ISG15 antiviral mechanism
- Interferon Signaling
- Inhibition of PKR
- Cytokine Signaling in Immune system
- Host Interactions with Influenza Factors
- Influenza Infection
- NS1 Mediated Effects on Host Pathways
- Antiviral mechanism by IFN-stimulated genes
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- Minocycline
- 5-[4-(1-Carboxymethyl-2-Oxo-Propylcarbamoyl)-Benzylsulfamoyl]-2-Hydroxy-Benzoic Acid
- 2-HYDROXY-5-(2-MERCAPTO-ETHYLSULFAMOYL)-BENZOIC ACID
- methyl (3S)-3-[(tert-butoxycarbonyl)amino]-4-oxopentanoate
- 1-METHYL-5-(2-PHENOXYMETHYL-PYRROLIDINE-1-SULFONYL)-1H-INDOLE-2,3-DIONE
- [N-(3-DIBENZYLCARBAMOYL-OXIRANECARBONYL)-HYDRAZINO]-ACETIC ACID
- 4-[5-(2-CARBOXY-1-FORMYL-ETHYLCARBAMOYL)-PYRIDIN-3-YL]-BENZOIC ACID
- (1S)-2-oxo-1-phenyl-2-[(1,3,4-trioxo-1,2,3,4-tetrahydroisoquinolin-5-yl)amino]ethyl acetate
- (1S)-1-(3-chlorophenyl)-2-oxo-2-[(1,3,4-trioxo-1,2,3,4-tetrahydroisoquinolin-5-yl)amino]ethyl acetate
- N-[3-(2-fluoroethoxy)phenyl]-N\'-(1,3,4-trioxo-1,2,3,4-tetrahydroisoquinolin-6-yl)butanediamide
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| CASP7 and EIF2AK2 |
caspase 7, apoptosis-related cysteine peptidase |
eukaryotic translation initiation factor 2-alpha kinase 2 |
- Activation of caspases through apoptosome-mediated cleavage
- Apoptotic cleavage of cellular proteins
- Apoptotic factor-mediated response
- SMAC binds to IAPs
- Apoptotic execution phase
- Programmed Cell Death
- SMAC-mediated dissociation of IAP:caspase complexes
- Cytochrome c-mediated apoptotic response
- SMAC-mediated apoptotic response
- Caspase-mediated cleavage of cytoskeletal proteins
- Intrinsic Pathway for Apoptosis
|
- ISG15 antiviral mechanism
- Interferon Signaling
- Inhibition of PKR
- Cytokine Signaling in Immune system
- Host Interactions with Influenza Factors
- Influenza Infection
- NS1 Mediated Effects on Host Pathways
- Antiviral mechanism by IFN-stimulated genes
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| CASP8 and EIF2AK2 |
caspase 8, apoptosis-related cysteine peptidase |
eukaryotic translation initiation factor 2-alpha kinase 2 |
- TRAIL signaling
- Death Receptor Signalling
- Caspase-8 activation by cleavage
- FasL/ CD95L signaling
- Activation, myristolyation of BID and translocation to mitochondria
- Caspase-mediated cleavage of cytoskeletal proteins
- Activated TLR4 signalling
- NOD1/2 Signaling Pathway
- Programmed Cell Death
- TRIF-mediated programmed cell death
- Innate Immune System
- Intrinsic Pathway for Apoptosis
- Regulation by c-FLIP
- Apoptotic cleavage of cellular proteins
- Dimerization of procaspase-8
- TRIF-mediated TLR3/TLR4 signaling
- Apoptotic execution phase
- MyD88-independent cascade
- RIG-I/MDA5 mediated induction of IFN-alpha/beta pathways
- Toll-Like Receptors Cascades
- Nucleotide-binding domain, leucine rich repeat containing receptor (NLR) signaling pathways
- Toll Like Receptor 4 (TLR4) Cascade
- Toll Like Receptor 3 (TLR3) Cascade
- NF-kB activation through FADD/RIP-1 pathway mediated by caspase-8 and -10
- Extrinsic Pathway
|
- ISG15 antiviral mechanism
- Interferon Signaling
- Inhibition of PKR
- Cytokine Signaling in Immune system
- Host Interactions with Influenza Factors
- Influenza Infection
- NS1 Mediated Effects on Host Pathways
- Antiviral mechanism by IFN-stimulated genes
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|
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| CASP10 and POLR2A |
caspase 10, apoptosis-related cysteine peptidase |
polymerase (RNA) II (DNA directed) polypeptide A, 220kDa |
- RIG-I/MDA5 mediated induction of IFN-alpha/beta pathways
- TRAIL signaling
- Death Receptor Signalling
- FasL/ CD95L signaling
- Programmed Cell Death
- NF-kB activation through FADD/RIP-1 pathway mediated by caspase-8 and -10
- Extrinsic Pathway
- Innate Immune System
|
- RNA Polymerase II Promoter Escape
- mRNA Splicing
- Formation of HIV-1 elongation complex containing HIV-1 Tat
- PIWI-interacting RNA (piRNA) biogenesis
- Nucleotide Excision Repair
- RNA Polymerase II Transcription Pre-Initiation And Promoter Opening
- RNA Polymerase II Transcription
- Abortive elongation of HIV-1 transcript in the absence of Tat
- HIV Infection
- Regulatory RNA pathways
- Formation of the Early Elongation Complex
- Tat-mediated elongation of the HIV-1 transcript
- Tat-mediated HIV elongation arrest and recovery
- Formation of transcription-coupled NER (TC-NER) repair complex
- RNA Pol II CTD phosphorylation and interaction with CE
- RNA Polymerase II Pre-transcription Events
- Dual incision reaction in TC-NER
- Influenza Life Cycle
- HIV elongation arrest and recovery
- HIV Life Cycle
- HIV Transcription Initiation
- Influenza Viral RNA Transcription and Replication
- RNA Pol II CTD phosphorylation and interaction with CE
- Transcriptional regulation of pluripotent stem cells
- RNA Polymerase II HIV Promoter Escape
- HIV Transcription Elongation
- POU5F1 (OCT4), SOX2, NANOG activate genes related to proliferation
- Transcriptional regulation by small RNAs
- Processing of Capped Intron-Containing Pre-mRNA
- mRNA Capping
- mRNA Splicing - Minor Pathway
- mRNA Splicing - Major Pathway
- MicroRNA (miRNA) biogenesis
- Influenza Infection
- Pausing and recovery of Tat-mediated HIV elongation
- Late Phase of HIV Life Cycle
- Formation of RNA Pol II elongation complex
- RNA Polymerase II Transcription Initiation And Promoter Clearance
- Pausing and recovery of HIV elongation
- Formation of HIV elongation complex in the absence of HIV Tat
- Transcription-coupled NER (TC-NER)
- Viral Messenger RNA Synthesis
- Formation of the HIV-1 Early Elongation Complex
- RNA Polymerase II Transcription Initiation
- Transcription of the HIV genome
- RNA Polymerase II Transcription Elongation
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| RUNX1T1 and HSP90AA1 |
runt-related transcription factor 1; translocated to, 1 (cyclin D-related) |
heat shock protein 90kDa alpha (cytosolic), class A member 1 |
|
- HSF1 activation
- Regulatory RNA pathways
- Signaling by EGFRvIII in Cancer
- Regulation of PLK1 Activity at G2/M Transition
- Influenza Life Cycle
- Influenza Viral RNA Transcription and Replication
- Constitutive Signaling by Ligand-Responsive EGFR Cancer Variants
- Uptake and actions of bacterial toxins
- EPH-Ephrin signaling
- Tetrahydrobiopterin (BH4) synthesis, recycling, salvage and regulation
- Fcgamma receptor (FCGR) dependent phagocytosis
- Recruitment of mitotic centrosome proteins and complexes
- Regulation of actin dynamics for phagocytic cup formation
- vRNP Assembly
- Influenza Infection
- Signaling by ERBB2
- Signaling by VEGF
- Signaling by EGFR in Cancer
- Sema3A PAK dependent Axon repulsion
- Mitotic G2-G2/M phases
- Uptake and function of diphtheria toxin
- PIWI-interacting RNA (piRNA) biogenesis
- Organelle biogenesis and maintenance
- Axon guidance
- Attenuation phase
- G2/M Transition
- VEGFA-VEGFR2 Pathway
- HSF1-dependent transactivation
- EPHA-mediated growth cone collapse
- Metabolism of nitric oxide
- VEGFR2 mediated vascular permeability
- Loss of Nlp from mitotic centrosomes
- Scavenging by Class F Receptors
- eNOS activation and regulation
- Innate Immune System
- Semaphorin interactions
- Signaling by Ligand-Responsive EGFR Variants in Cancer
- Assembly of the primary cilium
- Cellular response to heat stress
- Anchoring of the basal body to the plasma membrane
- Cell Cycle, Mitotic
- eNOS activation
- Loss of proteins required for interphase microtubule organization from the centrosome
- Centrosome maturation
- Constitutive Signaling by EGFRvIII
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|
- Rifabutin
- Nedocromil
- 9-Butyl-8-(2,5-Dimethoxy-Benzyl)-9h-Purin-6-Ylamine
- Geldanamycin
- 8-(2-Chloro-3,4,5-Trimethoxy-Benzyl)-2-Fluoro-9-Pent-4-Ylnyl-9h-Purin-6-Ylamine
- 9-Butyl-8-(3,4,5-Trimethoxybenzyl)-9h-Purin-6-Amine
- 4-(1,3-Benzodioxol-5-Yl)-5-(5-Ethyl-2,4-Dihydroxyphenyl)-2h-Pyrazole-3-Carboxylic Acid
- 17-Dmag
- 8-(2,5-Dimethoxy-Benzyl)-2-Fluoro-9h-Purin-6-Ylamine
- 8-(2,5-Dimethoxy-Benzyl)-2-Fluoro-9-Pent-9h-Purin-6-Ylamine
- Adenosine-5\'-Diphosphate
- 9-Butyl-8-(2-Chloro-3,4,5-Trimethoxy-Benzyl)-9h-Purin-6-Ylamine
- 4-(1h-Imidazol-4-Yl)-3-(5-Ethyl-2,4-Dihydroxy-Phenyl)-1h-Pyrazole
- 9-Butyl-8-(3-Methoxybenzyl)-9h-Purin-6-Amine
- 9-Butyl-8-(4-Methoxybenzyl)-9h-Purin-6-Amine
- 9-Butyl-8-(2,5-Dimethoxy-Benzyl)-2-Fluoro-9h-Purin-6-Ylamine
- 8-Benzo[1,3]Dioxol-,5-Ylmethyl-9-Butyl-2-Fluoro-9h-Purin-6-Ylamine
- 8-(2-Chloro-3,4,5-Trimethoxy-Benzyl)-9-Pent-4-Ylnyl-9h-Purin-6-Ylamine
- N-[4-(AMINOSULFONYL)BENZYL]-5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-1H-PYRAZOLE-4-CARBOXAMIDE
- N-(4-ACETYLPHENYL)-5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-1H-PYRAZOLE-4-CARBOXAMIDE
- 4-CHLORO-6-(4-{4-[4-(METHYLSULFONYL)BENZYL]PIPERAZIN-1-YL}-1H-PYRAZOL-5-YL)BENZENE-1,3-DIOL
- 5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-N-ETHYL-4-PIPERAZIN-1-YL-1H-PYRAZOLE-3-CARBOXAMIDE
- 5-(5-chloro-2,4-dihydroxyphenyl)-N-ethyl-4-[4-(morpholin-4-ylmethyl)phenyl]isoxazole-3-carboxamide
- 5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-N-ETHYL-4-(4-METHOXYPHENYL)ISOXAZOLE-3-CARBOXAMIDE
- 2-amino-4-[2,4-dichloro-5-(2-pyrrolidin-1-ylethoxy)phenyl]-N-ethylthieno[2,3-d]pyrimidine-6-carboxamide
- 4-CHLORO-6-(4-PIPERAZIN-1-YL-1H-PYRAZOL-5-YL)BENZENE-1,3-DIOL
- (3E)-3-[(phenylamino)methylidene]dihydrofuran-2(3H)-one
- 6-(3-BROMO-2-NAPHTHYL)-1,3,5-TRIAZINE-2,4-DIAMINE
- 3-({2-[(2-AMINO-6-METHYLPYRIMIDIN-4-YL)ETHYNYL]BENZYL}AMINO)-1,3-OXAZOL-2(3H)-ONE
- N-[(2-AMINO-6-METHYLPYRIMIDIN-4-YL)METHYL]-3-{[(E)-(2-OXODIHYDROFURAN-3(2H)-YLIDENE)METHYL]AMINO}BENZENESULFONAMIDE
- 5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-N-ETHYL-4-(4-METHOXYPHENYL)-1H-PYRAZOLE-3-CARBOXAMIDE
- 4-bromo-6-(6-hydroxy-1,2-benzisoxazol-3-yl)benzene-1,3-diol
- 4-[4-(2,3-DIHYDRO-1,4-BENZODIOXIN-6-YL)-3-METHYL-1H-PYRAZOL-5-YL]-6-ETHYLBENZENE-1,3-DIOL
- 4-chloro-6-{5-[(2-morpholin-4-ylethyl)amino]-1,2-benzisoxazol-3-yl}benzene-1,3-diol
- 8-(6-BROMO-BENZO[1,3]DIOXOL-5-YLSULFANYL)-9-(3-ISOPROPYLAMINO-PROPYL)-ADENINE
- 4-methyl-7,8-dihydro-5H-thiopyrano[4,3-d]pyrimidin-2-amine
- (5E,7S)-2-amino-7-(4-fluoro-2-pyridin-3-ylphenyl)-4-methyl-7,8-dihydroquinazolin-5(6H)-one oxime
- 8-BENZO[1,3]DIOXOL-,5-YLMETHYL-9-BUTYL-9H-
- 4-{[(2R)-2-(2-methylphenyl)pyrrolidin-1-yl]carbonyl}benzene-1,3-diol
- 2-(1H-pyrrol-1-ylcarbonyl)benzene-1,3,5-triol
- 2-[(2-methoxyethyl)amino]-4-(4-oxo-1,2,3,4-tetrahydro-9H-carbazol-9-yl)benzamide
- 4-(2-methoxyethoxy)-6-methylpyrimidin-2-amine
- 4-(2,4-dichlorophenyl)-5-phenyldiazenyl-pyrimidin-2-amine
- 3,6-DIAMINO-5-CYANO-4-(4-ETHOXYPHENYL)THIENO[2,3-B]PYRIDINE-2-CARBOXAMIDE
- 2-AMINO-4-(2,4-DICHLOROPHENYL)-N-ETHYLTHIENO[2,3-D]PYRIMIDINE-6-CARBOXAMIDE
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| RUNX1T1 and KPNA1 |
runt-related transcription factor 1; translocated to, 1 (cyclin D-related) |
karyopherin alpha 1 (importin alpha 5) |
|
- Vpr-mediated nuclear import of PICs
- ISG15 antiviral mechanism
- HIV Infection
- Host Interactions of HIV factors
- Interferon Signaling
- Apoptotic execution phase
- Integration of provirus
- Cytokine Signaling in Immune system
- Interactions of Vpr with host cellular proteins
- Influenza Infection
- Antiviral mechanism by IFN-stimulated genes
- Early Phase of HIV Life Cycle
- Influenza Life Cycle
- HIV Life Cycle
- Activation of DNA fragmentation factor
- Transport of Ribonucleoproteins into the Host Nucleus
- Apoptosis induced DNA fragmentation
- Programmed Cell Death
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| RUNX1T1 and KPNB1 |
runt-related transcription factor 1; translocated to, 1 (cyclin D-related) |
karyopherin (importin) beta 1 |
|
- Metabolism of lipids and lipoproteins
- ISG15 antiviral mechanism
- Nuclear import of Rev protein
- HIV Infection
- Interferon Signaling
- Apoptotic execution phase
- Host Interactions of HIV factors
- Cytokine Signaling in Immune system
- Interactions of Rev with host cellular proteins
- Influenza Infection
- Antiviral mechanism by IFN-stimulated genes
- Influenza Life Cycle
- Regulation of cholesterol biosynthesis by SREBP (SREBF)
- Activation of DNA fragmentation factor
- Transport of Ribonucleoproteins into the Host Nucleus
- Apoptosis induced DNA fragmentation
- Programmed Cell Death
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| CCNH and POLR2A |
cyclin H |
polymerase (RNA) II (DNA directed) polypeptide A, 220kDa |
- RNA Polymerase II Promoter Escape
- Formation of HIV-1 elongation complex containing HIV-1 Tat
- RNA Polymerase II Transcription Pre-Initiation And Promoter Opening
- RNA Polymerase I Chain Elongation
- RNA Polymerase I, RNA Polymerase III, and Mitochondrial Transcription
- Tat-mediated elongation of the HIV-1 transcript
- Cyclin E associated events during G1/S transition
- Formation of transcription-coupled NER (TC-NER) repair complex
- Dual incision reaction in TC-NER
- NoRC negatively regulates rRNA expression
- G1/S Transition
- Mitotic G1-G1/S phases
- S Phase
- Late Phase of HIV Life Cycle
- Formation of RNA Pol II elongation complex
- Global Genomic NER (GG-NER)
- RNA Polymerase II Transcription Initiation And Promoter Clearance
- Cyclin A:Cdk2-associated events at S phase entry
- Mitotic G2-G2/M phases
- Transcription of the HIV genome
- Nucleotide Excision Repair
- RNA Polymerase II Transcription
- RNA Polymerase I Transcription Initiation
- HIV Infection
- RNA Polymerase I Promoter Clearance
- Formation of the Early Elongation Complex
- G2/M Transition
- RNA Pol II CTD phosphorylation and interaction with CE
- RNA Polymerase II Pre-transcription Events
- HIV Transcription Initiation
- HIV Life Cycle
- RNA Pol II CTD phosphorylation and interaction with CE
- Cyclin A/B1 associated events during G2/M transition
- RNA Polymerase II HIV Promoter Escape
- HIV Transcription Elongation
- Dual incision reaction in GG-NER
- RNA Polymerase I Transcription
- mRNA Capping
- RNA Polymerase I Promoter Escape
- RNA Polymerase I Transcription Termination
- G1 Phase
- Epigenetic regulation of gene expression
- Negative epigenetic regulation of rRNA expression
- Cell Cycle, Mitotic
- Cyclin D associated events in G1
- Transcription-coupled NER (TC-NER)
- Formation of HIV elongation complex in the absence of HIV Tat
- Formation of the HIV-1 Early Elongation Complex
- Formation of incision complex in GG-NER
- RNA Polymerase II Transcription Initiation
- RNA Polymerase II Transcription Elongation
|
- RNA Polymerase II Promoter Escape
- mRNA Splicing
- Formation of HIV-1 elongation complex containing HIV-1 Tat
- PIWI-interacting RNA (piRNA) biogenesis
- Nucleotide Excision Repair
- RNA Polymerase II Transcription Pre-Initiation And Promoter Opening
- RNA Polymerase II Transcription
- Abortive elongation of HIV-1 transcript in the absence of Tat
- HIV Infection
- Regulatory RNA pathways
- Formation of the Early Elongation Complex
- Tat-mediated elongation of the HIV-1 transcript
- Tat-mediated HIV elongation arrest and recovery
- Formation of transcription-coupled NER (TC-NER) repair complex
- RNA Pol II CTD phosphorylation and interaction with CE
- RNA Polymerase II Pre-transcription Events
- Dual incision reaction in TC-NER
- Influenza Life Cycle
- HIV elongation arrest and recovery
- HIV Life Cycle
- HIV Transcription Initiation
- Influenza Viral RNA Transcription and Replication
- RNA Pol II CTD phosphorylation and interaction with CE
- Transcriptional regulation of pluripotent stem cells
- RNA Polymerase II HIV Promoter Escape
- HIV Transcription Elongation
- POU5F1 (OCT4), SOX2, NANOG activate genes related to proliferation
- Transcriptional regulation by small RNAs
- Processing of Capped Intron-Containing Pre-mRNA
- mRNA Capping
- mRNA Splicing - Minor Pathway
- mRNA Splicing - Major Pathway
- MicroRNA (miRNA) biogenesis
- Influenza Infection
- Pausing and recovery of Tat-mediated HIV elongation
- Late Phase of HIV Life Cycle
- Formation of RNA Pol II elongation complex
- RNA Polymerase II Transcription Initiation And Promoter Clearance
- Pausing and recovery of HIV elongation
- Formation of HIV elongation complex in the absence of HIV Tat
- Transcription-coupled NER (TC-NER)
- Viral Messenger RNA Synthesis
- Formation of the HIV-1 Early Elongation Complex
- RNA Polymerase II Transcription Initiation
- Transcription of the HIV genome
- RNA Polymerase II Transcription Elongation
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| CCNH and POLR2B |
cyclin H |
polymerase (RNA) II (DNA directed) polypeptide B, 140kDa |
- RNA Polymerase II Promoter Escape
- Formation of HIV-1 elongation complex containing HIV-1 Tat
- RNA Polymerase II Transcription Pre-Initiation And Promoter Opening
- RNA Polymerase I Chain Elongation
- RNA Polymerase I, RNA Polymerase III, and Mitochondrial Transcription
- Tat-mediated elongation of the HIV-1 transcript
- Cyclin E associated events during G1/S transition
- Formation of transcription-coupled NER (TC-NER) repair complex
- Dual incision reaction in TC-NER
- NoRC negatively regulates rRNA expression
- G1/S Transition
- Mitotic G1-G1/S phases
- S Phase
- Late Phase of HIV Life Cycle
- Formation of RNA Pol II elongation complex
- Global Genomic NER (GG-NER)
- RNA Polymerase II Transcription Initiation And Promoter Clearance
- Cyclin A:Cdk2-associated events at S phase entry
- Mitotic G2-G2/M phases
- Transcription of the HIV genome
- Nucleotide Excision Repair
- RNA Polymerase II Transcription
- RNA Polymerase I Transcription Initiation
- HIV Infection
- RNA Polymerase I Promoter Clearance
- Formation of the Early Elongation Complex
- G2/M Transition
- RNA Pol II CTD phosphorylation and interaction with CE
- RNA Polymerase II Pre-transcription Events
- HIV Transcription Initiation
- HIV Life Cycle
- RNA Pol II CTD phosphorylation and interaction with CE
- Cyclin A/B1 associated events during G2/M transition
- RNA Polymerase II HIV Promoter Escape
- HIV Transcription Elongation
- Dual incision reaction in GG-NER
- RNA Polymerase I Transcription
- mRNA Capping
- RNA Polymerase I Promoter Escape
- RNA Polymerase I Transcription Termination
- G1 Phase
- Epigenetic regulation of gene expression
- Negative epigenetic regulation of rRNA expression
- Cell Cycle, Mitotic
- Cyclin D associated events in G1
- Transcription-coupled NER (TC-NER)
- Formation of HIV elongation complex in the absence of HIV Tat
- Formation of the HIV-1 Early Elongation Complex
- Formation of incision complex in GG-NER
- RNA Polymerase II Transcription Initiation
- RNA Polymerase II Transcription Elongation
|
- RNA Polymerase II Promoter Escape
- mRNA Splicing
- Formation of HIV-1 elongation complex containing HIV-1 Tat
- PIWI-interacting RNA (piRNA) biogenesis
- Nucleotide Excision Repair
- RNA Polymerase II Transcription Pre-Initiation And Promoter Opening
- RNA Polymerase II Transcription
- Abortive elongation of HIV-1 transcript in the absence of Tat
- HIV Infection
- Regulatory RNA pathways
- Formation of the Early Elongation Complex
- Tat-mediated elongation of the HIV-1 transcript
- Tat-mediated HIV elongation arrest and recovery
- Formation of transcription-coupled NER (TC-NER) repair complex
- RNA Pol II CTD phosphorylation and interaction with CE
- RNA Polymerase II Pre-transcription Events
- Dual incision reaction in TC-NER
- Influenza Life Cycle
- HIV elongation arrest and recovery
- HIV Life Cycle
- HIV Transcription Initiation
- Influenza Viral RNA Transcription and Replication
- RNA Pol II CTD phosphorylation and interaction with CE
- Transcriptional regulation of pluripotent stem cells
- RNA Polymerase II HIV Promoter Escape
- HIV Transcription Elongation
- POU5F1 (OCT4), SOX2, NANOG activate genes related to proliferation
- Transcriptional regulation by small RNAs
- Processing of Capped Intron-Containing Pre-mRNA
- mRNA Capping
- mRNA Splicing - Minor Pathway
- mRNA Splicing - Major Pathway
- MicroRNA (miRNA) biogenesis
- Influenza Infection
- Pausing and recovery of Tat-mediated HIV elongation
- Late Phase of HIV Life Cycle
- Formation of RNA Pol II elongation complex
- RNA Polymerase II Transcription Initiation And Promoter Clearance
- Pausing and recovery of HIV elongation
- Formation of HIV elongation complex in the absence of HIV Tat
- Transcription-coupled NER (TC-NER)
- Viral Messenger RNA Synthesis
- Formation of the HIV-1 Early Elongation Complex
- RNA Polymerase II Transcription Initiation
- Transcription of the HIV genome
- RNA Polymerase II Transcription Elongation
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| CCNT1 and POLR2A |
cyclin T1 |
polymerase (RNA) II (DNA directed) polypeptide A, 220kDa |
- Loss of Function of TGFBR2 in Cancer
- Formation of HIV-1 elongation complex containing HIV-1 Tat
- RNA Polymerase II Transcription
- HIV Infection
- SMAD2/3 MH2 Domain Mutants in Cancer
- Tat-mediated elongation of the HIV-1 transcript
- Tat-mediated HIV elongation arrest and recovery
- TGFBR1 LBD Mutants in Cancer
- RNA Polymerase II Pre-transcription Events
- SMAD2/SMAD3:SMAD4 heterotrimer regulates transcription
- Transcriptional activity of SMAD2/SMAD3:SMAD4 heterotrimer
- HIV elongation arrest and recovery
- HIV Life Cycle
- Generic Transcription Pathway
- HIV Transcription Elongation
- TGFBR2 MSI Frameshift Mutants in Cancer
- SMAD2/3 Phosphorylation Motif Mutants in Cancer
- Loss of Function of SMAD2/3 in Cancer
- TGFBR2 Kinase Domain Mutants in Cancer
- Host Interactions of HIV factors
- Loss of Function of SMAD4 in Cancer
- Interactions of Tat with host cellular proteins
- TGFBR1 KD Mutants in Cancer
- Pausing and recovery of Tat-mediated HIV elongation
- Loss of Function of TGFBR1 in Cancer
- Late Phase of HIV Life Cycle
- Formation of RNA Pol II elongation complex
- Signaling by TGF-beta Receptor Complex
- Signaling by TGF-beta Receptor Complex in Cancer
- Pausing and recovery of HIV elongation
- Formation of HIV elongation complex in the absence of HIV Tat
- Transcription of the HIV genome
- SMAD4 MH2 Domain Mutants in Cancer
- RNA Polymerase II Transcription Elongation
|
- RNA Polymerase II Promoter Escape
- mRNA Splicing
- Formation of HIV-1 elongation complex containing HIV-1 Tat
- PIWI-interacting RNA (piRNA) biogenesis
- Nucleotide Excision Repair
- RNA Polymerase II Transcription Pre-Initiation And Promoter Opening
- RNA Polymerase II Transcription
- Abortive elongation of HIV-1 transcript in the absence of Tat
- HIV Infection
- Regulatory RNA pathways
- Formation of the Early Elongation Complex
- Tat-mediated elongation of the HIV-1 transcript
- Tat-mediated HIV elongation arrest and recovery
- Formation of transcription-coupled NER (TC-NER) repair complex
- RNA Pol II CTD phosphorylation and interaction with CE
- RNA Polymerase II Pre-transcription Events
- Dual incision reaction in TC-NER
- Influenza Life Cycle
- HIV elongation arrest and recovery
- HIV Life Cycle
- HIV Transcription Initiation
- Influenza Viral RNA Transcription and Replication
- RNA Pol II CTD phosphorylation and interaction with CE
- Transcriptional regulation of pluripotent stem cells
- RNA Polymerase II HIV Promoter Escape
- HIV Transcription Elongation
- POU5F1 (OCT4), SOX2, NANOG activate genes related to proliferation
- Transcriptional regulation by small RNAs
- Processing of Capped Intron-Containing Pre-mRNA
- mRNA Capping
- mRNA Splicing - Minor Pathway
- mRNA Splicing - Major Pathway
- MicroRNA (miRNA) biogenesis
- Influenza Infection
- Pausing and recovery of Tat-mediated HIV elongation
- Late Phase of HIV Life Cycle
- Formation of RNA Pol II elongation complex
- RNA Polymerase II Transcription Initiation And Promoter Clearance
- Pausing and recovery of HIV elongation
- Formation of HIV elongation complex in the absence of HIV Tat
- Transcription-coupled NER (TC-NER)
- Viral Messenger RNA Synthesis
- Formation of the HIV-1 Early Elongation Complex
- RNA Polymerase II Transcription Initiation
- Transcription of the HIV genome
- RNA Polymerase II Transcription Elongation
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