LMAN1

Gene Name		lectin, mannose-binding, 1
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Gene Ontology Annotations	Cellular Component	Golgi Membrane Endoplasmic Reticulum Membrane Endoplasmic Reticulum-Golgi Intermediate Compartment ER To Golgi Transport Vesicle Membrane Membrane Integral Component Of Membrane Sarcomere Endoplasmic Reticulum-Golgi Intermediate Compartment Membrane Host Cell Perinuclear Region Of Cytoplasm Extracellular Vesicular Exosome
	Molecular Function	Protein Binding Mannose Binding Metal Ion Binding Unfolded Protein Binding
	Biological Process	Protein Folding ER To Golgi Vesicle-mediated Transport Endoplasmic Reticulum Organization Golgi Organization Blood Coagulation Positive Regulation Of Organelle Organization Protein N-linked Glycosylation Via Asparagine Protein Exit From Endoplasmic Reticulum Early Endosome To Golgi Transport Post-translational Protein Modification Cellular Protein Metabolic Process
Pathways		Defective ALG2 causes ALG2-CDG (CDG-1i) Diseases of glycosylation Defective ALG3 causes ALG3-CDG (CDG-1d) Post-translational protein modification Defective DPAGT1 causes DPAGT1-CDG (CDG-1j) and CMSTA2 Defective ALG14 causes congenital myasthenic syndrome (ALG14-CMS) Transport to the Golgi and subsequent modification Defective MGAT2 causes MGAT2-CDG (CDG-2a) Defective ALG1 causes ALG1-CDG (CDG-1k) Defective B4GALT1 causes B4GALT1-CDG (CDG-2d) Defective ALG6 causes ALG6-CDG (CDG-1c) Defective RFT1 causes RFT1-CDG (CDG-1n) Defective MOGS causes MOGS-CDG (CDG-2b) Asparagine N-linked glycosylation Defective ALG8 causes ALG8-CDG (CDG-1h) Defective ALG9 causes ALG9-CDG (CDG-1l) Defective MPDU1 causes MPDU1-CDG (CDG-1f) Defective MAN1B1 causes MRT15 Defective ALG12 causes ALG12-CDG (CDG-1g) Diseases associated with N-glycosylation of proteins Defective ALG11 causes ALG11-CDG (CDG-1p)
Drugs
Diseases
GWAS
Protein-protein Interactions		4 interactors: APP BCAP31 F8 MCFD2
Entrez ID		3998
HPRD ID		03338
Ensembl ID		ENSG00000074695
Uniprot IDs		P49257
PDB IDs		3A4U 3LCP 4GKX 4GKY
Enriched GO Terms of Interacting Partners?		Endoplasmic Reticulum Calcium Ion Homeostasis Vesicle-mediated Transport Platelet Degranulation Positive Regulation Of Peptidase Activity Synaptic Growth At Neuromuscular Junction Platelet Activation Collateral Sprouting In Absence Of Injury Collateral Sprouting Axon Midline Choice Point Recognition Cellular Calcium Ion Homeostasis Positive Regulation Of Proteolysis Smooth Endoplasmic Reticulum Calcium Ion Homeostasis Protein Localization To Endoplasmic Reticulum Exit Site Calcium Ion Homeostasis Axon Choice Point Recognition Exocytosis Neuron Remodeling Regulation Of Endopeptidase Activity Positive Regulation Of Mitochondrial Calcium Ion Concentration Negative Regulation Of Endoplasmic Reticulum Calcium Ion Concentration Cellular Metal Ion Homeostasis Regulation Of Peptidase Activity Blood Coagulation Hemostasis Transport Cellular Cation Homeostasis Calcium-mediated Signaling Using Intracellular Calcium Source Cellular Ion Homeostasis Establishment Of Localization In Cell Metal Ion Homeostasis Blood Coagulation, Intrinsic Pathway Secretion By Cell Mitochondrial Calcium Ion Homeostasis Cellular Chemical Homeostasis Cellular Copper Ion Homeostasis Ion Homeostasis Regulation Of Body Fluid Levels Wound Healing Copper Ion Homeostasis Suckling Behavior Cellular Localization Secretion Positive Regulation Of G2/M Transition Of Mitotic Cell Cycle Regulation Of Proteolysis Cell Activation Cellular Homeostasis Neuron Maturation MRNA Polyadenylation Regulation Of Epidermal Growth Factor-activated Receptor Activity Response To Wounding
Tagcloud ?		abnormal abnormality cargo cis compartment direct electroretinogram er ergic eyes gm130 golgi grasp65 histology homeostasis intermediate location markers months mouse nrl photoreceptor retina rhodopsin selectively taken transmembrane transport transports