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Validated All-in-One™ qPCR Primer for ITGA3(NM_002204.4) Search again
Product ID:
HQP130538
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CD49C, FRP-2, GAP-B3, GAPB3, ILNEB, JEB7, MSK18, VCA-2, VL3A, VLA3a
Gene Description:
integrin subunit alpha 3
Target Gene Accession:
NM_002204.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
The protein encoded by this gene belongs to the family of integrins. Integrins are heterodimeric integral membrane proteins composed of an alpha chain and a beta chain, and function as cell surface adhesion molecules. This gene encodes alpha 3 subunit, which undergoes post-translational cleavage in the extracellular domain to yield disulfide-linked light and heavy chains that join with beta 1 subunit to form an integrin that interacts with many extracellular-matrix proteins. Alternatively spliced transcript variants encoding different isoforms have been identified for this gene. [provided by RefSeq].
Gene References into function
- Data demonstrate that multiple tetraspanin (transmembrane 4 superfamily) proteins such as CD151 are palmitoylated, and that palmitoylation is not required for cd151-alpha3beta1 integrin association.
- Human prostate tumors display on their cell surface the alpha6beta1 and/or alpha3beta1 integrins
- initial adhesion of endometrial cells to mesothelium is not mediated by alpha(3)beta(1)integrin
- Integrin-alpha 3 sub-unit participates the process of regulating growth of meningiomas.
- expression of alpha3 integrin subunit is responsible for differentiation-associated changes in cells behavior in terminally differentiated oral keratinocytes
- signaling through both constitutively expressed alpha2 integrin and Matrigel-induced alpha3 integrin expression is required to acquire a differentiated phenotype in Caco-2 cells.
- Data show that macrophage stimulating protein (MSP) and its receptor (Ron) induce phosphorylation of both Ron and alpha6beta4 integrin, and result in activation of alpha3beta1 integrin.
- Disulfide bonding patterns of the integrin alpha 3 chain are described; the alpha chain displays differences in the disulfide patterns of those bonds near their C-terminal regions linking the heavy and light chains.
- Data demonstrate that alpha6beta4 integrin mediates pancreatic epithelial cell adhesion to Netrin-1, whereas recruitment of alpha6beta4 and alpha3beta1 regulate the migration of putative pancreatic progenitors on Netrin-1.
- ligand-binding specificities of integrin alpha3beta1 and alpha6beta1
- alpha3beta1 integrin binding to laminin-5 depends on its proteolytic processing
- results suggest that a direct interaction occurs between the Adenovirus penton base protein and the integrin receptor alpha3beta1 in vitro and in vivo
- results show how laterally associated EWI-2 might regulate alpha3beta1 function in disease and development, and demonstrate how tetraspanin proteins can assemble multiple nontetraspanin proteins into functional complexes
- alpha3beta1, alpha4beta1 and alphaVbeta1 integrins may play an important role in the implantation process
- Data suggest that the early arrest of tumor cells in the pulmonary vasculature through interaction of alpha3beta1 integrin with laminin-5 in exposed basement membrane provides a basis for cell arrest during pulmonary metastasis.
- Alpha 3 beta 1 integrin is necessary and sufficient for maximal keratinocyte survival on laminin-5.
- cAMP-Epac-Rap1 pathway regulates cell spreading and cell adhesion to laminin-5 through the alpha3beta1 integrin but not the alpha6beta4 integrin
- Results indicate that CD151 association modulates the ligand-binding activity of integrin alpha3beta1 through stabilizing its activated conformation not only with purified proteins but also in a physiological context.
- Beta ig-h3 induces keratinocyte differentiation via modulation of involucrin and transglutaminase expression through the integrin alpha3beta1 and the phosphatidylinositol 3-kinase/Akt signaling pathway
- KSHV gB can activate VEGFR-3 on the microvascular endothelium and modulate endothelial cell migration and proliferation via an interaction between the alpha3beta1 integrin and the VEGFR-3 receptor
- alpha3beta1 integrin binding results in a suppression of the interleukin-1 signaling pathway leading to the activation of NF-(kappa)B
- alpha3, alpha5, and alpha6 beta1 integrins are expressed in ductal cells at 8 weeks, before glucagon- and insulin-immunoreactive cells bud off in fetal pancrea.
- the signaling network involving Smad-dependent TGFbeta, PKCdelta, and integrin alpha2beta1/alpha3beta1, regulates cell spreading, motility, and invasion of the SNU16mAd gastric carcinoma cell variant
- phenotypic conversion and reversion of bladder cancer cells is controlled by a glycosynapse 3 microdomain through GM3-mediated interaction of alpha3beta1 integrin with CD9
- localized expression of the integrin alpha3 protein is regulated at the level of RNA localization by MBNL1; integrin alpha3 transcripts are physically associated with MLP1 in cells and MLP1 binds to a specific ACACCC motif in the integrin alpha3 3' UTR
- Thus, the integrin/Src pathway negatively regulates the induction of long-term plasticity at inhibitory synapses on a cerebellar Purkinje cells.
- Data show that alpha6 and alpha3 integrin subunits interact with laminin 5 to increase expression of E-cadherin, and suggest that phosphoinositide 3-kinase (PI 3-kinase) activation plays a key role in this cross-talk.
- Our data show that alpha3beta1 integrin function may be altered by glycosylation, that both subunits contribute to these changes, and glycosylation may be considered a newly found mechanism in the regulation of integrin function.
- Results suggest that loss of E-cadherin function is linked to regulation of cell-cell and cell-matrix adhesion, based in part on cell surface expression of alpha2, alpha3 and beta1 integrins.
- decreased podocyte expression of alpha3beta1 integrins is closely related with podocyte depletion, glomerular sclerosis, and daily protein loss in patients with primary focal glomerulosclerosis
- TGF-beta1 stimulates hepatoma cells to express a higher level of alpha3 integrin by transcriptional upregulation via Ets transcription factors and to exhibit a more invasive phenotype.
- This study supports matrix-induced clustering of alpha3beta1 integrin promotes uPAR/alpha3beta1 interaction; potentiating cellular signal transduction pathways culminating in activation of uPA expression and enhanced uPA-dependent invasive behavior.
- EWI proteins EWI-2 and EWI-F, alpha3beta1 and alpha6beta4 integrins, and protein palmitoylation have contrasting effects on cell surface CD9 organization
- Both integrin alpha3beta1- and alpha6beta4-dependent cell adhesion to laminin-5 were also impaired in CD151-silenced cells.
- Slug regulates integrin alpha3, beta1, and beta4 expression and cell proliferation in human epidermal keratinocytes
- integrin alpha3beta1 is a receptor for the alpha3NC1 domain and transdominantly inhibits integrin alphavbeta3 activation
- Acquisition of multiple antitumor drugs was accompanied by a drastically reduced expression of alpha3beta1 in the adenocarcinoma cells.
- Binding of Borrelia burgdorferi to integrin alpha 3 beta 1 results in release of inflammatory mediators from human chondrocytes and is proposed as a Toll-like receptor-independent pathway for activation of the innate immune response.
- Chondrocytes with low chondrogenic capacity expressed higher levels of IGF-1, MMP-2, aggrecanase 2, while chondrocytes with high chondrogenic capacity expressed higher levels of CD44, CD151, and CD49c.
- Integrin-mediated adhesion via alpha3beta1, but not alpha6beta4 integrin, supports cell survival through EGFR by signaling downstream to Erk.
- These results indicate that binding of the alpha3beta1 integrin results in a suppression in the activation of the IL-1 induced intracellular signaling pathway from JNK to AP-1.
- findings suggest an important role of integrin alpha2beta1, alpha3beta1, and alpha5beta1 in the architectural characteristics of ameloblastomas and adenomatoid odentogenic tumor
- Beta1 and alpha3 integrins are functionally important receptors for type 1 pili-expressing bacteria within the urinary tract and possibly at other sites within the host.
- identification of alpha3beta1 as the predominant integrin and laminin receptor in glioma cells, and as a brain invasion-mediating integrin
- These results strongly suggest that enhanced expression of alpha3beta1 integrin on hepatocellular carcinoma cells is directly involved in their malignant phenotypes such as invasion and metastasis.
- Increase in ITGA3 is associated with lymph node metastasis in squamous cell carcinoma of the tongue
- Both integrins, v3 and v5, are involved in the glioma cell radioresistance through the integrin-linked kinase (ILK) and the small GTPase RhoB, at least by regulating the radiation-induced mitotic cell death.
- CD151 regulates integrin alpha3beta1 functions in two independent aspects: potentiation of integrin alpha3beta1-mediated cell adhesion and promotion of integrin alpha3beta1-stimulated signaling events involving tyrosine phosphorylation
- Results suggest that HAb18G/CD147 enhances the invasion and metastatic potentials of human hepatoma cells via integrin alpha3beta1-mediated FAK-paxillin and FAKPI3K-Ca(2+) signal pathways.
- Src overexpression downregulates alpha3 integrin total protein expression and localization to the cell surface of HCT116 colon cancer cells. This indicates that Src activity may enhance metastasis by altering alpha3 integrin expression.
- Glomerular deposition of C5b-9 and a positive correlation with the intensity of tubular alpha3beta1-integrin suggests a possible implication in the development of tubulointerstitial fibrosis.