Database for Annotation, Visualization and Integrated Discovery 2.1
National Institute of Allergy and Infectious Disease
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par-3 family cell polarity regulator(PARD3) par-3 family cell polarity regulator(PARD3) Related Genes Homo sapiens
CHROMOSOME 10,
CYTOBAND 10p11.22-p11.21, 6p12.2,
ENSEMBL_GENE_ID ENSG00000148498,
GENERIF_SUMMARY findings demonstrated that G-protein-activated phospholipase C-beta interacts with cell polarity proteins Par3 and Par6 to form protein complexes and to mediate downstream signal transduction, fine-tuning mechanism of Par3 in epithelial tight junction assembly controlled by the EGF receptor-SFK signaling pathway., We provide evidence for the existence of a distinct PAR protein complex in endothelial cells. Both PAR-3 and PAR-6 associate directly with the adherens junction protein vascular endothelial cadherin (VE-cadherin)., Par3 is a novel component of the DNA-PK complex that implicates an unexpected link of cell polarity to double-strand DNA break repair., Because Numb interacts with the aPKC binding partner PAR-3, we propose a model in which polarized Numb phosphorylation contributes to cell migration by directing integrin endocytosis to the leading edge, Two polarity proteins, Par3 and Par6, are also required for EC lumen and tube formation, as they establish EC polarity through their association with Cdc42 and atypical PKC., Neph1-Nephrin proteins bind the Par3-Par6-atypical protein kinase C (aPKC) complex to regulate podocyte cell polarity, identified 10 potential novel binding proteins of PDZ domains of Par3 in Jurkat cells, Results suggest that deletion and reduced expression of PARD3 may be a novel mechanism that drives the progression of ESCC., Cell polarity factor Par3 binds SPTLC1 and modulates monocyte serine palmitoyltransferase activity and chemotaxis, Pard-3 and AS3 genes are mutationally inactivated in prostate cancer cells., Data show that Aurora A interacts directly with the atypical protein kinase C binding domain of Par3 and phosphorylates it at serine 962., The results suggest that Par3 directly interacts with FAK and PI3-kinase, enhancing their activities for polarized cell migration., Par3 controls epithelial spindle orientation by aPKC-mediated phosphorylation of apical Pins., Factors-derived from preeclapsia placentas not only interrupt junction protein VE-cadherin distribution, but also perturb polarity protein PARD-3 expression and distribution in vascular endothelium, Data show that DDR1 coordinates the Par3/Par6 cell-polarity complex through its carboxy terminus, binding PDZ domains in Par3 and Par6., there was no association of MAGI2 and PARD3 with IBD., Data indicate that both tumor focality and Par3/Par6/atypical protein kinase C (APKC) expression were significantly associated with tumor recurrence., Changes in cell polarity proteins Par-3 and PP-1 are associated with altered expression and assembly of tight junction proteins claudin-2, -3, -5 and -7 and ZO-1, causing paracellular leakage in active coeliac disease., A VE-cadherin-PAR3-alpha-catenin complex regulates the Golgi localization and activity of cytosolic phospholipase A(2)alpha in endothelial cells.(, genetic association studies in a Chinese Han population, The scaffolding adaptor GAB1 interacts with two polarity proteins, PAR1 and PAR3., Par3 is identified as a regulator of signaling pathways relevant to invasive breast cancer., Suggest that loss of Par3 promotes metastatic behaviour of ErbB2-induced breast tumour epithelial cells by decreasing cell-cell cohesion., Data show that increased partitioning defective 3 (Par-3) expression is associated with distant metastasis and poor survival rates in patients with hepatocellular carcinoma (HCC)., Our results suggest that PAR-3 has a role in the clinical aggressiveness of cell Renal Cell Carcinoma, The PAR polarity complex of PARD3, PARD6, and an atypical protein kinase C (aPKC) regulate several aspects of neuronal migration.[review], A cytoplasmic expression of PAR-3 is therefore implicated in worse clinical and pathological cancer features in clear cell renal cell carcinoma and could be useful to identify patients with high-risk tumors., PAR3 and aPKC control the organization of the Golgi through CLASP2 phosphorylation., Par-3 plays an important role in the modulation of intestinal barrier function by regulating delivery of occludin as well as suppression of MLC phosphorylation., PAR3-mutant proteins exhibit a relative reduction in the ability to mediate formation of tight junctions and actin-based protrusions and activate STAT3 at cell confluence., Shp2 promotes metastasis of prostate cancer by attenuating the PAR3/PAR6/aPKC polarity protein complex and enhancing epithelial-to-mesenchymal transition, study indicated a potential molecular basis for cell growth-promoting function of PARD3 by modulating the Hippo pathway signaling in response to cell contact and cell polarity signals, Knockdown of the polarity protein Par3 reversed the effects of Galpha13 knockdown on cell-cell adhesion and proteolytic invasion in three-dimensional collagen.,
OFFICIAL_GENE_SYMBOL PARD3,
SP_COMMENT alternative products:Additional isoforms seem to exist. As a matter of fact, alternatively spliced products seem to fall into two broad groups: one group, which includes the longest continuous ORF but which may also include molecules lacking some middle domains, has a single TM element and is likely to be associated with the plasma membrane. The other group lacks a TM domain and thus its members may be secreted, disease:Defects in PKHD1 are the cause of polycystic kidney disease autosomal recessive (ARPKD) [MIM:263200]. ARPKD is a severe form of polycystic kidney disease affecting the kidneys and the hepatic biliary tract. The clinical spectrum is widely variable, with most cases presenting during infancy. The fetal phenotypic features classically include enlarged and echogenic kidneys, as well as oligohydramnios secondary to a poor urine output. Up to 50% of the affected neonates die shortly after birth, as a result of severe pulmonary hypoplasia and secondary respiratory insufficiency. In the subset that survives the perinatal period, morbidity and mortality are mainly related to severe systemic hypertension, renal insufficiency, and portal hypertension due to portal-tract fibrosis., domain:Contains a conserved N-terminal oligomerization domain (NTD) that is involved in oligomerization and is essential for proper subapical membrane localization., function:Adapter protein involved in asymmetrical cell division and cell polarization processes. Seems to play a central role in the formation of epithelial tight junctions. Association with PARD6B may prevent the interaction of PARD3 with F11R/JAM1, thereby preventing tight junction assembly. The PARD6-PARD3 complex links GTP-bound Rho small GTPases to atypical protein kinase C proteins., function:May be a receptor protein that acts in collecting-duct and biliary differentiation., miscellaneous:Antibodies against PARD3 are present in sera from patients with cutaneous T-cell lymphomas., PTM:Phosphorylated by PRKCZ. EGF-induced Tyr-1127 phosphorylation mediates dissociation from LIMK2., sequence caution:Contaminating sequence. Potential poly-A sequence., similarity:Belongs to the PAR3 family., similarity:Contains 12 IPT/TIG domains., similarity:Contains 3 PDZ (DHR) domains., similarity:Contains 9 PbH1 repeats., subcellular location:Localized along the cell-cell contact region. Colocalizes with PARD6A and PRKCI at epithelial tight junctions. Colocalizes with the cortical actin that overlays the meiotic spindle during metaphase I and metaphase II., subunit:Interacts with PARD6A and PARD6B. Isoform 2, but not at least isoform 3 interacts with PRKCZ. Interacts with PRCKI (By similarity). Part of a complex with PARD6A or PARD6B, PRKCI or PRKCZ and CDC42 or RAC1. Interacts with F11R/JAM1 (By similarity). Component of a complex whose core is composed of ARHGAP17, AMOT, MPP5/PALS1, INADL/PATJ and PARD3/PAR3. Interacts with LIMK2., tissue specificity:Predominantly expressed in fetal and adult kidney. Also present in the adult pancreas, but at much lower levels. Detectable in fetal and adult liver. Rather indistinct signal in fetal brain., tissue specificity:Widely expressed.,