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Lgl1 (zeige Klra7 Proteine) forms two distinct complexes in vivo, Lgl1 (zeige Klra7 Proteine)-NMIIA and Lgl1 (zeige Klra7 Proteine)-Par6alpha-aPKCzeta (zeige PRKCZ Proteine), and that the formation of these complexes is affected by the phosphorylation state of Lgl1 (zeige Klra7 Proteine).
Our results provide the first in vivo characterization of RalA (zeige rala Proteine) 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 (zeige DCTN1 Proteine) complex, and requires Cdc42 (zeige CDC42 Proteine), Par6 and Par3 (zeige F2RL2 Proteine).
PAR6 has a role in forming primordial follicles in mouse ovary
Rin (zeige RIT2 Proteine) and Rit (zeige RIT1 Proteine) Bind to PAR6 GTP (zeige AK3 Proteine)-dependently and regulate cell transformation
Par6alpha-mediated inhibition of insulin (zeige INS Proteine)-dependent glycogen (zeige GYS1 Proteine) synthesis in C2C12 cells depends on the direct interaction of Par6alpha with aPKC and on aPKC-mediated T34 phosphorylation of Akt1 (zeige AKT1 Proteine).
In addition to regulating Par-6-aPKC localization, Cdc42 (zeige CDC42 Proteine) increases aPKC activity by relieving Par-6 inhibition.
Neph1 (zeige NEPH1 Proteine)-Nephrin (zeige NPHS1 Proteine) proteins bind the Par3 (zeige F2RL2 Proteine)-Par6-atypical protein kinase C (zeige PRKCZ Proteine) (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 (zeige TGFB1 Proteine)-Par6 polarity pathway has a role in breast cancer progression
We first demonstrate that Hook2 (zeige HOOK2 Proteine) is essential for the polarized Golgi re-orientation towards the migration front. Depletion of Hook2 (zeige HOOK2 Proteine) results in a decrease of PAR6alpha at the centrosome during cell migration, while overexpression of Hook2 (zeige HOOK2 Proteine) in cells induced the formation of aggresomes with the recruitment of PAR6alpha, aPKC and PAR3 (zeige F2RL2 Proteine)
Roles of partitioning-defective protein 6 (Par6) and its complexes in the proliferation, migration and invasion of cancer cells
Shp2 (zeige PTPN11 Proteine) promotes metastasis of prostate cancer by attenuating the PAR3 (zeige F2RL2 Proteine)/PAR6/aPKC polarity protein complex and enhancing epithelial-to-mesenchymal transition
TGFbeta (zeige TGFB1 Proteine) 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 (zeige PRKCZ Proteine). The p-Par6-aPKCzeta (zeige PRKCZ Proteine) complex is important for cell migration and invasion.
Data indicate that both tumor focality and Par3 (zeige F2RL2 Proteine)/Par6/atypical protein kinase C (zeige PRKCZ Proteine) (APKC) expression were significantly associated with tumor recurrence.
BDNF (zeige BDNF Proteine) can regulate formation of functional synapses by increasing the expression of the RhoA (zeige RHOA Proteine) inhibitors, Par6C and Rnd3 (zeige RND3 Proteine).
Morg1 (zeige wdr83 Proteine) facilitates Par6-aPKC binding to Crb3 (zeige CRB3 Proteine) 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 (zeige PRKCZ Proteine) kinase activity, as well as an association with PAR6, were found to be important for PAR6 phosphorylation.
Pak6 (zeige PAK6 Proteine) is a binding partner and a outatuve effector protein for the atypical rho GTPase (zeige RACGAP1 Proteine) cdc42 (zeige CDC42 Proteine) homologous protein.
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 (zeige CSTB Proteine)-2.1/2/CDK-1 (zeige CDK1 Proteine) antagonize CUL-2 (zeige CUL2 Proteine) 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 (zeige CDH1 Proteine), 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 (zeige AFG3L2 Proteine) polarity arises from coupling of advective transport by flowing cell cortex to a multistable PAR (zeige AFG3L2 Proteine) 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 (zeige F2RL1 Proteine) and PAR-6, which localize to opposing PAR (zeige AFG3L2 Proteine) 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 ligand, is required for PAR-6 function in C. elegans
PAR (zeige AFG3L2 Proteine) 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 (zeige CDC42 Proteine)-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