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Lgl1 forms two distinct complexes in vivo, Lgl1-NMIIA and Lgl1-Par6alpha-aPKCzeta (Montrer PRKCZ Kits ELISA), and that the formation of these complexes is affected by the phosphorylation state of Lgl1.
Our results provide the first in vivo characterization of RalA (Montrer rala Kits ELISA) function in the mammalian brain and highlight a novel
The nucleus of a myoblast moves rapidly after fusion towards the central myotube nuclei which is driven by microtubules and dynein/dynactin (Montrer DCTN1 Kits ELISA) complex, and requires Cdc42 (Montrer CDC42 Kits ELISA), Par6 and Par3 (Montrer F2RL2 Kits ELISA).
PAR6 has a role in forming primordial follicles in mouse ovary
Rin (Montrer RIT2 Kits ELISA) and Rit (Montrer RIT1 Kits ELISA) Bind to PAR6 GTP (Montrer AK3 Kits ELISA)-dependently and regulate cell transformation
Par6alpha-mediated inhibition of insulin (Montrer INS Kits ELISA)-dependent glycogen (Montrer GYS1 Kits ELISA) synthesis in C2C12 cells depends on the direct interaction of Par6alpha with aPKC and on aPKC-mediated T34 phosphorylation of Akt1 (Montrer AKT1 Kits ELISA).
In addition to regulating Par-6-aPKC localization, Cdc42 (Montrer CDC42 Kits ELISA) increases aPKC activity by relieving Par-6 inhibition.
Neph1 (Montrer NEPH1 Kits ELISA)-Nephrin (Montrer NPHS1 Kits ELISA) proteins bind the Par3 (Montrer F2RL2 Kits ELISA)-Par6-atypical protein kinase C (Montrer PRKCZ Kits ELISA) (aPKC) complex to regulate podocyte cell polarity
The aPKC-PAR3 complex associates with the nephrin-podocin complex in podocytes through direct interaction between PAR3 and nephrin, and the kinase activity of aPKC is required for the appropriate distribution of nephrin and podocin in podocytes.
the TGFbeta (Montrer TGFB1 Kits ELISA)-Par6 polarity pathway has a role in breast cancer progression
Shp2 (Montrer PTPN11 Kits ELISA) promotes metastasis of prostate cancer by attenuating the PAR3 (Montrer F2RL2 Kits ELISA)/PAR6/aPKC polarity protein complex and enhancing epithelial-to-mesenchymal transition
TGFbeta (Montrer TGFB1 Kits ELISA) induced Par6 phosphorylation on Ser345 and its recruitment to the leading edge of the membrane ruffle in migrating PC-3U cells, where it colocalised with aPKCzeta (Montrer PRKCZ Kits ELISA). The p-Par6-aPKCzeta (Montrer PRKCZ Kits ELISA) complex is important for cell migration and invasion.
Data indicate that both tumor focality and Par3 (Montrer F2RL2 Kits ELISA)/Par6/atypical protein kinase C (Montrer PRKCZ Kits ELISA) (APKC) expression were significantly associated with tumor recurrence.
BDNF (Montrer BDNF Kits ELISA) can regulate formation of functional synapses by increasing the expression of the RhoA (Montrer RHOA Kits ELISA) inhibitors, Par6C and Rnd3 (Montrer RND3 Kits ELISA).
Morg1 (Montrer wdr83 Kits ELISA) facilitates Par6-aPKC binding to Crb3 (Montrer CRB3 Kits ELISA) for definition of apical identity of epithelial cells.
Par6 negatively regulates trophoblast fusion via its roles on tight junctions and cytoskeleton dynamics and provide novel insight into the contribution of this polarity marker in altered trophoblast cell fusion typical of preeclampsia.
Atypical protein kinase C (Montrer PRKCZ Kits ELISA) kinase activity, as well as an association with PAR6, were found to be important for PAR6 phosphorylation.
Pak6 (Montrer PAK6 Kits ELISA) is a binding partner and a outatuve effector protein for the atypical rho GTPase (Montrer RACGAP1 Kits ELISA) cdc42 (Montrer CDC42 Kits ELISA) homologous protein.
Data show that DDR1 coordinates the Par3 (Montrer F2RL2 Kits ELISA)/Par6 cell-polarity complex through its carboxy terminus, binding PDZ (Montrer INADL Kits ELISA) domains in Par3 (Montrer F2RL2 Kits ELISA) and Par6.
Par6alpha controls centrosome organization through its association with the dynactin (Montrer DCTN1 Kits ELISA) subunit p150(Glued (Montrer DCTN1 Kits ELISA)).
we find that vab-1 lies in the same genetic pathway as cdc-42 and is responsible for polarizing CDC-42 activity to the medial tip. Together, these data establish a previously uncharacterized role for polarized CDC-42, in conjunction with PAR-6, PAR-3 and an Eph receptor(vab-1), during epithelial intercalation.
Our results support a model in which CYB (Montrer CSTB Kits ELISA)-2.1/2/CDK-1 (Montrer CDK1 Kits ELISA) antagonize CUL-2 (Montrer CUL2 Kits ELISA) activity to promote stabilization of PAR-6 levels during polarization of the early C. elegans embryo.
the arcade cell epithelium polarizes by a PAR-6-mediated pathway that is independent of E-cadherin (Montrer CDH1 Kits ELISA), beta-integrin and beta-laminin.
PAR-3 and PAR-6 function in cytokinesis may be partially redundant and play a role in the maintenance of DYN-1 in the cleavage furrow.
evidence PAR (Montrer AFG3L2 Kits ELISA) polarity arises from coupling of advective transport by flowing cell cortex to a multistable PAR (Montrer AFG3L2 Kits ELISA) reaction-diffusion system; advection in active, flowing medium provides mechanism for mechanically templated pattern formation in development
Centrosomes localize apically by first moving toward lateral foci of the conserved polarity proteins PAR-3 and PAR-6, then move together with these foci toward the future apical surface. Embryos lacking PAR-3 fail to localize their centrosomes apically.
PAR-2 (Montrer F2RL1 Kits ELISA) and PAR-6, which localize to opposing PAR (Montrer AFG3L2 Kits ELISA) domains, undergo exchange between well mixed cytoplasmic populations and laterally diffusing membrane-associated states
Binding to PKC-3, but not to PAR-3 or to a conventional PDZ domain (Montrer INADL Kits ELISA) ligand, is required for PAR-6 function in C. elegans
PAR (Montrer AFG3L2 Kits ELISA) proteins function in both apicobasal and anterior-posterior asymmetry during the first few cell cycles of embryogenesis.
CDC-37-mediated inhibition of the CDC-42 (Montrer CDC42 Kits ELISA)-dependent binding site and PAR-3-mediated release of this inhibition provide a key mechanism for the anterior accumulation of PAR-6.
This gene is a member of the PAR6 family and encodes a protein with a PSD95/Discs-large/ZO1 (PDZ) domain and a semi-Cdc42/Rac interactive binding (CRIB) domain. This cell membrane protein is involved in asymmetrical cell division and cell polarization processes as a member of a multi-protein complex. The protein also has a role in the epithelial-to-mesenchymal transition (EMT) that characterizes the invasive phenotype associated with metastatic carcinomas. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.
par-6 partitioning defective 6 homolog alpha (C. elegans)
, partitioning defective 6 homolog alpha
, PAR-6 alpha
, Tax interaction protein 40
, partitioning defective protein 6A
, Tax-interacting protein 40
, par-6 partitioning defective 6 homolog alpha
, partitioning defective-6 homolog alpha
, partitioning-defective protein 6
, tax interaction protein 40