F8 and LMAN1

Number of citations of the paper that reports this interaction (PMID 14629470)
8

Data Source:
HPRD (in vivo)

		F8	LMAN1
Gene Name		coagulation factor VIII, procoagulant component	lectin, mannose-binding, 1
Image
Gene Ontology Annotations	Cellular Component	Extracellular Region Extracellular Space Plasma Membrane Platelet Alpha Granule Lumen	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	Serine-type Endopeptidase Activity Copper Ion Binding Protein Binding Oxidoreductase Activity	Protein Binding Mannose Binding Metal Ion Binding Unfolded Protein Binding
	Biological Process	Platelet Degranulation Proteolysis Acute-phase Response Blood Coagulation Blood Coagulation, Intrinsic Pathway Platelet Activation Oxidation-reduction 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		Common Pathway Intrinsic Pathway Response to elevated platelet cytosolic Ca2+ Platelet degranulation Platelet activation, signaling and aggregation Formation of Fibrin Clot (Clotting Cascade)	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		Drotrecogin alfa Coagulation Factor IX
Diseases
GWAS		Antineutrophil cytoplasmic antibody-associated vasculitis ( 22808956) Red blood cell traits ( 23446634)
Protein-Protein Interactions		16 interactors: ASGR2 CALR CANX F10 F2 F9 GGA1 HSPA5 LMAN1 LRP1 MCFD2 PHYH PROC PROS1 UBQLN1 VWF	4 interactors: APP BCAP31 F8 MCFD2
Entrez ID		2157	3998
HPRD ID		02384	03338
Ensembl ID		ENSG00000185010	ENSG00000074695
Uniprot IDs		P00451	P49257
PDB IDs		1CFG 1D7P 1FAC 1IQD 2R7E 3CDZ 3HNB 3HNY 3HOB 3J2Q 3J2S 4BDV	3A4U 3LCP 4GKX 4GKY
Enriched GO Terms of Interacting Partners?		Post-translational Protein Modification Peptidyl-glutamic Acid Carboxylation Blood Coagulation Hemostasis Blood Coagulation, Intrinsic Pathway Regulation Of Body Fluid Levels Wound Healing Peptidyl-amino Acid Modification Vesicle-mediated Transport Response To Wounding Protein N-linked Glycosylation Via Asparagine Protein N-linked Glycosylation Protein Metabolic Process Blood Coagulation, Extrinsic Pathway Protein Activation Cascade Negative Regulation Of Blood Coagulation Platelet Activation Negative Regulation Of Coagulation Glycoprotein Metabolic Process Negative Regulation Of Wound Healing Response To Stress Platelet Degranulation Regulation Of Blood Coagulation Protein Glycosylation Macromolecule Glycosylation Glycosylation Cellular Protein Modification Process Receptor-mediated Endocytosis Regulation Of Wound Healing Cellular Protein Metabolic Process Glycoprotein Biosynthetic Process Establishment Of Localization In Cell Response To Endoplasmic Reticulum Stress Fibrinolysis Secretion By Cell Proteolysis Transport Leukocyte Migration Cellular Localization Regulation Of Cell Migration Activation Of Signaling Protein Activity Involved In Unfolded Protein Response Positive Regulation Of Nuclease Activity Regulation Of Cell Motility Chaperone-mediated Protein Folding Secretion Peptide Antigen Assembly With MHC Class I Protein Complex Beta-amyloid Clearance Regulation Of Protein Folding In Endoplasmic Reticulum Positive Regulation Of Phospholipase C-activating G-protein Coupled Receptor Signaling Pathway Endocytosis	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 ?		absent ba betac csf f3 gm gmr gmralpha gmrbeta granulocyte heterodimeric magnitude mitogenesis next phenylalanine phosphorylaiton proliferate prominent regenerate residues restored shc shp2 stat5 sufficient tyrosine y577 y612 y695	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
Tagcloud (Difference) ?		absent ba betac csf f3 gm gmr gmralpha gmrbeta granulocyte heterodimeric magnitude mitogenesis next phenylalanine phosphorylaiton proliferate prominent regenerate residues restored shc shp2 stat5 sufficient tyrosine y577 y612 y695	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
Tagcloud (Intersection) ?