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抗Mouse (Murine) PARD3 抗体:
抗Rat (Rattus) PARD3 抗体:
抗Human PARD3 抗体:
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 2 Pubmed References
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.
HTT (显示 HTT 抗体) is required for the apical localization of PAR3 (显示 F2RL2 抗体)-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 (显示 SMEK1 抗体) substrate and demonstrate that Smek1 (显示 SMEK1 抗体) suppresses its activity.
Par3 (显示 F2RL2 抗体) (and protein kinase C zeta (显示 PRKCZ 抗体)) are activated in neurons when binding to N2-proteoglygan.
Suggest that loss of Par3 (显示 F2RL2 抗体) promotes metastatic behaviour of ErbB2 (显示 ERBB2 抗体)-induced breast tumour epithelial cells by decreasing cell-cell cohesion.
Par3 (显示 F2RL2 抗体) is identified as a regulator of signaling pathways relevant to invasive breast cancer.
The nucleus of a myoblast moves rapidly after fusion towards the central myotube nuclei which is driven by microtubules and dynein/dynactin (显示 DCTN1 抗体) complex, and requires Cdc42 (显示 CDC42 抗体), Par6 (显示 PARD6A 抗体) and Par3 (显示 F2RL2 抗体).
Data suggest that aPKC phosphorylates JAM-A (显示 F11R 抗体) at S285 to regulate cell-cell contact maturation, TJ formation, and single lumen specification.
Brain-derived neurotrophic factor (BDNF (显示 BDNF 抗体)) induces polarized signaling of small GTPase (显示 RACGAP1 抗体) (Rac1) protein at the onset of Schwann cell myelination through partitioning-defective 3 (Par3 (显示 F2RL2 抗体)) protein.
Report a willin(FRMD6 (显示 FRMD6 抗体))/Par3 (显示 F2RL2 抗体)-aPKC-ROCK pathway that controls epithelial apical morphology.
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 (显示 F2RL2 抗体) in tumorigenic transformation of human cervical keratinocytes.
Results suggest that Par3 (显示 F2RL2 抗体) expression is likely involved in ovarian cancer progression, especially in peritoneal metastasis, probably through modulating IL-6 (显示 IL6 抗体) /STAT3 (显示 STAT3 抗体) 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 (显示 F2RL2 抗体) and SNAIL (显示 SNAI1 抗体) in development of KSHV-induced B-cells cancers
PAR-3 (显示 F2RL2 抗体) protein expression is frequently lost in primary esophageal squamous cell carcinoma and loss of the PAR-3 (显示 F2RL2 抗体) protein is associated with aggressive clinicopathological features.
Taken together, these results suggest that the Par3 (显示 F2RL2 抗体) regulates invasion and metastasis in pancreatic cancers by controlling tight junction assembly via Tiam1 (显示 TIAM1 抗体).
Knockdown of the polarity protein Par3 reversed the effects of Galpha13 (显示 GNA13 抗体) knockdown on cell-cell adhesion and proteolytic invasion in three-dimensional collagen.
Shp2 (显示 PTPN11 抗体) promotes metastasis of prostate cancer by attenuating the PAR3 (显示 F2RL2 抗体)/PAR6 (显示 PARD6A 抗体)/aPKC polarity protein complex and enhancing epithelial-to-mesenchymal transition
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 (显示 RAB11A 抗体) are necessary for lumen formation in the neural rod.
Brain-derived neurotrophic factor (BDNF (显示 BDNF 抗体)) induces polarized signaling of small GTPase (显示 RACGAP1 抗体) (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 (显示 TDGF1 抗体), the PDZ (显示 INADL 抗体) domains, and the C-terminal portion of the protein.
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.
partitioning-defective protein 3 homolog
, partitioning defective 3 homolog
, par-3 partitioning defective 3 homolog (C. elegans)
, atypical PKC isotype-specific-interacting protein
, ephrin-interacting protein
, 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)
, CTCL tumor antigen se2-5
, atypical PKC isotype-specific interacting protein
, par-3 family cell polarity regulator alpha
, par-3 partitioning defective 3 homolog