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Human Polyclonal PARD3 Primary Antibody for ICC, IF - ABIN4343686
Whiteman, Fan, Harder, Walton, Liu, Soofi, Fogg, Hershenson, Dressler, Deutsch, Gumucio, Margolis: Crumbs3 is essential for proper epithelial development and viability. in Molecular and cellular biology 2013
Show all 3 Pubmed References
PAR-3 controls microtubule stability via inhibition of GSK3beta in a dose-dependent manner. The dose-dependent effect of PAR-3 on GSK3beta phosphorylation is due to antagonism between the aPKC/PAR-3 and the aPKC/GSK3beta complexes.
Therefore, Porphyromonas gingivalis not only directly stimulates CXCL14 expression via PAR-3 but also promotes its expression by antagonising EGF signalling.
The expression of Pard3 was increased by the inhibition of miR-483, but TGF-beta1-induced cell migration and invasion were decreased by miR-483 inhibition. A dual-luciferase reporter assay determined that Pard3 expression was downregulated when targeted with miR-483. The epithelial-mesenchymal transition (EMT), as well as Tiam1-Rac signaling, was induced by TGF-beta1, which was decreased by the overexpression of Pard3.
Studies indicate that the PAR3-PAR6-aPKC complex are important for the establishment of neuronal polarity [Review].
that this heterozygotic microdeletion showed no tissue specificity and led to defective expression of PARD3
The authors identified a tumor-suppressive property function of Par3 in human cervical cancer and the lost Par3 expression may be a marker of poor prognosis.
We first demonstrate that Hook2 is essential for the polarized Golgi re-orientation towards the migration front. Depletion of Hook2 results in a decrease of PAR6alpha at the centrosome during cell migration, while overexpression of Hook2 in cells induced the formation of aggresomes with the recruitment of PAR6alpha, aPKC and PAR3
elevated expression of Par3 promotes PCa metastasis via KIBRA sequestration-mediated inactivation of the Hippo pathway to upregulate expression of pro-metastatic genes.
reduced expression of PKCzeta/Pard3/Pard6 contributes to non-small-cell lung cancer epithelial-mesenchymal transition, invasion, and chemoresistance.
PARD3 might play a tumor suppressor role in esophageal squamous cell carcinoma.
Loss of Par3 promotes metastatic behavior in lung adenocarcinoma cells through 14-3-3zeta protein.
Studies suggest that rare deleterious variants of PARD3 in the aPKC-binding region contribute to human cranial neural tube defect (NTD).
These data highlight the importance of the carboxy-terminal motif of the E6 protein and downregulation of PAR3 in tumorigenic transformation of human cervical keratinocytes.
Results suggest that Par3 expression is likely involved in ovarian cancer progression, especially in peritoneal metastasis, probably through modulating IL-6 /STAT3 signaling.
reduced keratinocytes Par3 function fosters a permissive P-cadherin-dependent niche for melanocytes transformation, invasion, and metastasis.
These results demonstrate the importance of Par3 and SNAIL in development of KSHV-induced B-cells cancers
PAR-3 protein expression is frequently lost in primary esophageal squamous cell carcinoma and loss of the PAR-3 protein is associated with aggressive clinicopathological features.
Taken together, these results suggest that the Par3 regulates invasion and metastasis in pancreatic cancers by controlling tight junction assembly via Tiam1.
Knockdown of the polarity protein Par3 reversed the effects of Galpha13 knockdown on cell-cell adhesion and proteolytic invasion in three-dimensional collagen.
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.
Loss of endothelial PAR-3 disrupts regional axial cell polarity and increases pro-inflammatory response of endothelial cells.
mammary morphogenesis is dependent on the ability of Par3 to directly bind aPKC
The structure of par3-PDZ3 peptide bound to the C-terminal tail of vascular endothelial cadherin clearly shows that both canonical and distal interactions are utilized in binding and suggests a mechanism for ligand specificity within the polarity network.
results suggest that ERK2 phosphorylates Par3 and inhibits its binding with KIF3A, thereby controlling Par3 transport and neuronal polarity
Polycystin-1 binds Par3/PKCalpha and controls convergent extension during renal tubular morphogenesis.
Rassf5 and Ndr1 or Ndr2 kinases regulate neuronal polarity through Par3 phosphorylation.
support for the hitherto untested model that Par3-mInsc and Galphai3 act cooperatively to polarize LGN and promote perpendicular divisions
this study demonstrates a mechanism by which loss of Par3 promotes proliferation and tumorigenesis, which supports a tumor-suppressive function for Par3 in the mammary epithelium.
Loss of PAR3 triggers increased production of interleukin-6, which induces STAT3 signaling in an autocrine manner.
Par3 is the long-sought exocyst receptor required for targeted membrane-protein delivery.
Epidermal aPKClambda and Par3 promote a tumor-permissive environment.
Loss of Par3 promotes prostatic tumorigenesis by enhancing cell growth and changing cell division modes
radial glial progenitor behavior and cortical development are controlled by temporally distinct actions of partitioning-defective 3 (PARD3) in concert with dynamic HIPPO signaling
Par3A function is either dispensable for slit diaphragm integrity, or compensatory mechanisms and a high redundancy of the different polarity proteins
HTT is required for the apical localization of PAR3-aPKC during epithelial morphogenesis in virgin, pregnant, and lactating mice.
Authors identify the cell polarity protein Par3, a negative regulator of neuronal differentiation, as a Smek1 substrate and demonstrate that Smek1 suppresses its activity.
Par3 (and protein kinase C zeta) are activated in neurons when binding to N2-proteoglygan.
Suggest that loss of Par3 promotes metastatic behaviour of ErbB2-induced breast tumour epithelial cells by decreasing cell-cell cohesion.
Par3 is identified as a regulator of signaling pathways relevant to invasive breast cancer.
Data show that angiomotin like 2a (AmotL2) and par-3 family cell polarity regulator alpha b (Par3) form a protein complex controlling actin filament induction from adherens junctions.
Pard3 mediates contact inhibition between neural crest cells and promotes timely myelin gene expression but is not essential for neural crest migration or myelination.
these results demonstrate a novel role of Par3 during neural crest migration, which is likely to be conserved in other processes that involve contact inhibition of locomotion such as cancer invasion or cell dispersion.
Pard3 and Rab11a are necessary for lumen formation in the neural rod.
Brain-derived neurotrophic factor (BDNF) induces polarized signaling of small GTPase (Rac1) protein at the onset of Schwann cell myelination through partitioning-defective 3 (Par3) protein.
Study demonstrates that the microtubule cytoskeleton gradually transitions from a radial to linear organization during neurulation and that microtubules function in conjunction with the polarity protein Pard3 to mediate centrosome positioning.
Agouti signaling (ASIP) genes exist in many species in lower vertebrates and were most probably present in early stages of vertebrate evolution.
Apical localization of ASIP in neuroepithelial cells involves the oligomerization domain CR1, the PDZ domains, and the C-terminal portion of the protein.
Par3 physically associated with Prickle3 and promoted its apical localization.
This gene encodes a member of the PARD protein family. PARD family members interact with other PARD family members and other proteins\; they affect asymmetrical cell division and direct polarized cell growth. Multiple alternatively spliced transcript variants have been described for this gene.
CTCL tumor antigen se2-5
, atypical PKC isotype-specific interacting protein
, atypical PKC isotype-specific-interacting protein
, par-3 family cell polarity regulator alpha
, par-3 partitioning defective 3 homolog
, partitioning defective 3 homolog
, atypical PKC-specific binding protein
, atypical PKC-specific-binding protein
, partitioning-defective 3 homolog
, three-PDZ containing protein similar to C. elegans PAR3 (partitioning defect)
, partitioning-defective protein 3 homolog
, par-3 partitioning defective 3 homolog (C. elegans)
, ephrin-interacting protein
, partitioning-defective 3 protein
, par-3 family cell polarity regulator S homeolog