Selected-GenAtlas references	SOURCE	GeneCards	NCBI Gene	Swiss-Prot	Orphanet	Ensembl
	HGNC	UniGene	Nucleotide	OMIM		UCSC

Home Page

FLASH GENE

Symbol

ITGB3

contributors: mct - updated : 27-06-2017

HGNC name	integrin, beta 3 (platelet glycoprotein IIIa, antigen CD61)
HGNC id	6156

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

RNA

TRANSCRIPTS	type	messenger

identification nb exons type bp product Protein kDa AA specific expression Year Pubmed NM_000212 15 - 4894 NP_000203 87.1 788 - Jin (1998)

EXPRESSION

Type

widely

expressed in	(based on citations)
organ(s)	System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Endocrine thyroid       highly Urinary kidney       highly

cells

System Cell Pubmed Species Stage Rna symbol Blood/Hematopoietic megakaryocyte Homo sapiens Blood/Hematopoietic platelet Homo sapiens not specific mast cell Homo sapiens Skeleton osteoblast

cell lineage

cell lines

fluid/secretion

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	six N terminal domains highly conserved between ITGBx
	a transmembrane (1TM) segment
	a cytoplasmic segment containing potential phosphorylation sites
	four cys rich repeats

conjugated

GlycoP

mono polymer

heteromer , dimer

isoforms

Precursor

HOMOLOGY

intraspecies

paralog to ITGB1

Homologene

FAMILY

integrin beta chain family

CATEGORY

adhesion , antigen , receptor

SUBCELLULAR LOCALIZATION	plasma membrane
	intracellular
	intracellular,nucleus

basic FUNCTION	cell surface adhesion receptor for fibronectin, fibrinogen, vitronectin, prothrombin, thrombospondin and others, mediating cell-adhesion to extra cellular matrix or to other cells, through hetero dimerization and connecting to the cytoskeleton and various signaling molecules within cells
	collectively, ITGA2B /ITGB3 in mast cells plays an important part in fibrinogen (FB)-associated, chronic inflammation and innate immune responses
	required for iron transportation during enamel formation
	neurite elongation promoted by vascular endothelial cells requires ITGB3
	inhibits LPS-induced autophagy in cardiomyocytes, and the inhibition of AKT1 signaling might be an important mechanism in this process
	expression of ITGB3, as well as tumor-produced factors associated with bone destruction (GLI2 and PTHRP), significantly increased with matrix rigidity
	rigid mineralized bone matrix can alter gene expression and bone destruction in an ITGB3/TGFB1-dependent manner

CELLULAR PROCESS

cell communication

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

a component

dimerizing with ITGA2B, ITGAV (see symbols)

INTERACTION

DNA

RNA

small molecule

protein	ITGA2B, ITGAV
	may interact with SLC6A4 in mediating autism susceptibility
	interacting with FOXC2
	MARCKSL1 downregulation by ITGB3 is not required for increased cell spreading but instead is a secondary effect of increased cell spreading
	HOXA10 activates ITGB3 transcription in myeloid progenitor cells and differentiating phagocytes
	interaction between Trp110 of ITGA2B and Arg261 of ITGB3 is critical for ITGA2B/ITGB3 integrity and outside-in signaling-related functions
	PTK2B was rapidly phosphorylated and activated in platelets adherent to fibrinogen through integrin ITGA2B/ITGB3
	deoxyribose-1-phosphate (dRP) is a novel autocrine amplifier of platelet activity, which acts on platelet redox levels and modulates ITGA2B/ITGB3
	constitutive interaction between ITGB3 and SRC kinase
	SPRY4 overexpression resulted in decreased ITGB3 protein levels in a post-transcriptional manner in part by modulating its tyrosine phosphorylation by SRC
	ITGB3 is a modulator of serotonergic systems via genetic interactions with the 5-HT transporter gene (SLC6A4)
	serine/threonine phosphatases regulate platelet ITGA2B/ITGB3 integrin receptor outside-in signaling mechanisms and clot retraction
	protein ubiquitination promotes megakaryopoiesis via degrading SKIL, an inhibitor of ITGB3 expression, strengths the roles of ubiquitination in cellular differentiation
	CDK11A is an anti-metastatic gene in ESR1-positive breast cancer and that the regulation of ITGB3 by CDK11 via the repression of ESR1 signaling may constitute part of a signaling pathway underlying breast cancer invasion
	loss of traction force on ligand-bound ITGB3 causes recruitment of DAB2/clathrin, resulting in endocytosis of integrins

cell & other

REGULATION

activated by

FERMT3 (role of FERMT3 phosphorylation in ITGB3 activation, providing a basis for functional differences between FERMT3 and the two other kindlin paralogs)

Other

regulated by NFATC1

ASSOCIATED DISORDERS

corresponding disease(s)

GT3

related resource

Glanzmann Thrombasthenia Database

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function tumoral     --low   in human hepatocellular carcinoma cells (Wu 2009) constitutional     --low   significantly reduced ITGB3 expression compared to controls, in recurrent pregnancy loss constitutional     --over   ITGA2B/ITGB3 is significantly higher in atopic myelitis (AM) patients than in controls as well as in females compared with males constitutional germinal mutation     gain of function activating mutations in ITGA2B and ITGB3 represent the etiology of a subset of congenital macrothrombocytopenias

Susceptibility

in association with PAI1 in susceptibility to myocardial infarction in Finnish population (see PAI1) to cardiovascular disease to neonatal autoimmune thrombocytopenia, post transfusion to autism

Variant & Polymorphism SNP	98 C>T in susceptibility to preeclampsia
	Leu 33 associated with lower serotonin levels and with autism

Candidate gene
Marker
Therapy target
	System Type Disorder Pubmed cancer digestive liver reconstitution of ITGB3 in hepatocellular carcinoma may be a potential therapeutic approach to inhibit aggressive growth of liver cancer neurology neurodegenerative alzheimer ITGA2B/ITGB3 complex activation could be a putative prognostic biomarker for the rate of cognitive decline and a potential new treatment target in Alzheimer patients cancer metastases   ITGB3 inhibitors are a potential therapeutic approach for blocking tumor transition to a bone destructive phenotype

ANIMAL & CELL MODELS