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radial glial progenitor behavior and cortical development are controlled by temporally distinct actions of partitioning-defective 3 (PARD3) in concert with dynamic HIPPO signaling
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 蛋白) is required for the apical localization of PAR3 (显示 F2RL2 蛋白)-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 蛋白) substrate and demonstrate that Smek1 (显示 SMEK1 蛋白) suppresses its activity.
Par3 (显示 F2RL2 蛋白) (and protein kinase C zeta (显示 PRKCZ 蛋白)) are activated in neurons when binding to N2-proteoglygan.
Suggest that loss of Par3 (显示 F2RL2 蛋白) promotes metastatic behaviour of ErbB2 (显示 ERBB2 蛋白)-induced breast tumour epithelial cells by decreasing cell-cell cohesion.
Par3 (显示 F2RL2 蛋白) 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 蛋白) complex, and requires Cdc42 (显示 CDC42 蛋白), Par6 (显示 PARD6A 蛋白) and Par3 (显示 F2RL2 蛋白).
Data suggest that aPKC phosphorylates JAM-A (显示 F11R 蛋白) at S285 to regulate cell-cell contact maturation, TJ formation, and single lumen specification.
Brain-derived neurotrophic factor (BDNF (显示 BDNF 蛋白)) induces polarized signaling of small GTPase (显示 RACGAP1 蛋白) (Rac1) protein at the onset of Schwann cell myelination through partitioning-defective 3 (Par3 (显示 F2RL2 蛋白)) protein.
The authors identified a tumor-suppressive property function of Par3 (显示 F2RL2 蛋白) in human cervical cancer and the lost Par3 (显示 F2RL2 蛋白) expression may be a marker of poor prognosis.
We first demonstrate that Hook2 (显示 HOOK2 蛋白) is essential for the polarized Golgi re-orientation towards the migration front. Depletion of Hook2 (显示 HOOK2 蛋白) results in a decrease of PAR6alpha (显示 PARD6A 蛋白) at the centrosome during cell migration, while overexpression of Hook2 (显示 HOOK2 蛋白) in cells induced the formation of aggresomes with the recruitment of PAR6alpha (显示 PARD6A 蛋白), aPKC and PAR3 (显示 F2RL2 蛋白)
elevated expression of Par3 (显示 F2RL2 蛋白) promotes PCa (显示 FLVCR1 蛋白) metastasis via KIBRA (显示 WWC1 蛋白) sequestration-mediated inactivation of the Hippo pathway to upregulate expression of pro-metastatic genes.
reduced expression of PKCzeta (显示 PRKCZ 蛋白)/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 (显示 F2RL2 蛋白) promotes metastatic behavior in lung adenocarcinoma cells through 14-3-3zeta (显示 YWHAZ 蛋白) 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 (显示 F2RL2 蛋白) in tumorigenic transformation of human cervical keratinocytes.
Results suggest that Par3 (显示 F2RL2 蛋白) expression is likely involved in ovarian cancer progression, especially in peritoneal metastasis, probably through modulating IL-6 (显示 IL6 蛋白) /STAT3 (显示 STAT3 蛋白) signaling.
reduced keratinocytes Par3 function fosters a permissive P-cadherin-dependent niche for melanocytes transformation, invasion, and metastasis.
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 蛋白) are necessary for lumen formation in the neural rod.
Brain-derived neurotrophic factor (BDNF (显示 BDNF 蛋白)) induces polarized signaling of small GTPase (显示 RACGAP1 蛋白) (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.
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