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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 (Montrer HTT Protéines) is required for the apical localization of PAR3 (Montrer F2RL2 Protéines)-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 (Montrer SMEK1 Protéines) substrate and demonstrate that Smek1 (Montrer SMEK1 Protéines) suppresses its activity.
Par3 (Montrer F2RL2 Protéines) (and protein kinase C zeta (Montrer PRKCZ Protéines)) are activated in neurons when binding to N2-proteoglygan.
Suggest that loss of Par3 (Montrer F2RL2 Protéines) promotes metastatic behaviour of ErbB2 (Montrer ERBB2 Protéines)-induced breast tumour epithelial cells by decreasing cell-cell cohesion.
Par3 (Montrer F2RL2 Protéines) 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 (Montrer DCTN1 Protéines) complex, and requires Cdc42 (Montrer CDC42 Protéines), Par6 (Montrer PARD6A Protéines) and Par3 (Montrer F2RL2 Protéines).
Data suggest that aPKC phosphorylates JAM-A (Montrer F11R Protéines) at S285 to regulate cell-cell contact maturation, TJ formation, and single lumen specification.
Brain-derived neurotrophic factor (BDNF (Montrer BDNF Protéines)) induces polarized signaling of small GTPase (Montrer RACGAP1 Protéines) (Rac1) protein at the onset of Schwann cell myelination through partitioning-defective 3 (Par3 (Montrer F2RL2 Protéines)) protein.
Report a willin(FRMD6 (Montrer FRMD6 Protéines))/Par3 (Montrer F2RL2 Protéines)-aPKC-ROCK pathway that controls epithelial apical morphology.
PARD3 might play a tumor suppressor role in esophageal squamous cell carcinoma.
Loss of Par3 (Montrer F2RL2 Protéines) promotes metastatic behavior in lung adenocarcinoma cells through 14-3-3zeta (Montrer YWHAZ Protéines) 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 (Montrer F2RL2 Protéines) in tumorigenic transformation of human cervical keratinocytes.
Results suggest that Par3 (Montrer F2RL2 Protéines) expression is likely involved in ovarian cancer progression, especially in peritoneal metastasis, probably through modulating IL-6 (Montrer IL6 Protéines) /STAT3 (Montrer STAT3 Protéines) 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 (Montrer F2RL2 Protéines) and SNAIL (Montrer SNAI1 Protéines) in development of KSHV-induced B-cells cancers
PAR-3 (Montrer F2RL2 Protéines) protein expression is frequently lost in primary esophageal squamous cell carcinoma and loss of the PAR-3 (Montrer F2RL2 Protéines) protein is associated with aggressive clinicopathological features.
Taken together, these results suggest that the Par3 (Montrer F2RL2 Protéines) regulates invasion and metastasis in pancreatic cancers by controlling tight junction assembly via Tiam1 (Montrer TIAM1 Protéines).
Knockdown of the polarity protein Par3 reversed the effects of Galpha13 (Montrer GNA13 Protéines) knockdown on cell-cell adhesion and proteolytic invasion in three-dimensional collagen.
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 (Montrer RAB11A Protéines) are necessary for lumen formation in the neural rod.
Brain-derived neurotrophic factor (BDNF (Montrer BDNF Protéines)) induces polarized signaling of small GTPase (Montrer RACGAP1 Protéines) (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