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The adaptor proteins Crk and Crk-like (Crkl (Montrer CRKL Kits ELISA)), with which Dock proteins are known to interact physically, are also required for myoblast fusion.
The results suggest the involvement of Crk adaptor proteins in the early stages of T cell activation in which Crk might help recruiting effector proteins to the vicinity of the phospho-CD3zeta (Montrer CD247 Kits ELISA) and contribute to the fine-tuning of the TCR/CD3 (Montrer CD3 Kits ELISA)-coupled signal transduction pathways.
Study investigated structures and thermodynamics of the interactions mediated by N-terminal Src homology 3 domain of CrkII and proline-rich motifs (PRMs) of cAbl kinase, highlight the role of interfacial water molecules and the conformational entropy in the SH3:PRM interactions
CrkII mediates IGF-1 (Montrer IGF1 Kits ELISA) signaling and further balances pancreatic ductal adenocarcinoma biological behaviors via Erk1/2 (Montrer MAPK1/3 Kits ELISA) and Akt (Montrer AKT1 Kits ELISA) pathway
In individuals with class I 17p13.3 microduplications including CRK, we recommend biochemical evaluation of the growth hormone axis. Providers caring for these patients should be aware of their possible risk for the development of central precocious puberty.
Crk Tyr251 phosphorylation regulate invasive cell phenotypes in glioblastoma.
CsA (Montrer ERCC8 Kits ELISA) and FK506 might interfere with selected effector T cell functions via a CrkII-, but not CrkI-dependent mechanisms.
Studied the role of PAK1/Crk axis in transduction of the oncogenic KRAS signal in non-small cell lung cancer (NSCLC).
in human c-CrkII, movement at position 239 and strain at position 272 are not tolerated because the beta-branched residues Ile239 and Val272 restrain the backbone mobility and thus destabilize the cis (Montrer CISH Kits ELISA) Pro238 form.
Data indicate the role of tyrosine phosphorylation in regulating modular domain utilization in v-crk sarcoma virus CT10 oncogene homolog (avian) protein (Crk).
evidence uncovered essential roles of CRK in invasive bladder cancer through the hepatocyte growth factor (Montrer HGF Kits ELISA)/c-Met/CRK feedback loop for epithelial-mesenchymal transition induction
the data suggest that CCRK (Montrer CDK20 Kits ELISA) positively regulates the kinetics by which ciliary proteins such as Smoothened and Gli2 (Montrer GLI2 Kits ELISA) are imported into the cilium, and that the efficiency of ciliary recruitment allows for potent responses to Hedgehog (Montrer SHH Kits ELISA) signaling over long time periods.
results suggest that Crk and CrkL (Montrer CRKL Kits ELISA) play essential overlapping roles in fibroblast growth.
both Crk and CrkL are required for the acquisition of cellular transformation by v-fos, whereas Crk plays a more prominent role than CrkL in v-ras-induced transformation.
results support a model in which Dok1 (Montrer DOK1 Kits ELISA) phosphorylation normally suppresses localized Ras pathway activity in Crk-transformed cells via recruitment and/or activation of RasGAP (Montrer RASA1 Kits ELISA)
Differential migration of CRK/CRKL (Montrer CRKL Kits ELISA)-deficient T cells resulted in efficient graft-versus-leukemia responses with minimal graft-versus-host disease in mice.
Crk1 (Montrer MAPK14 Kits ELISA)/2 and CrkL (Montrer CRKL Kits ELISA) are physically linked, functionally complement each other during podocyte foot process spreading, and together are required for developing typical foot process architecture.
Data suggest that interactions between Crk (proto-oncogene (Montrer RAB1A Kits ELISA) proteins c-crk) and Sos1 (Son of Sevenless homolog 1 (Montrer SOS1 Kits ELISA)) involve electrostatic interactions at binding sites.
Results suggest that Crk and CrkL (Montrer CRKL Kits ELISA) have critical roles in cell structure and motility by maintaining cytoskeletal integrity.
The v-Crk-myosin-1c interaction, which modulates membrane dynamics by regulating Rac1 activity, is crucial for cell adhesion and spreading.
The authors cloned SH2 domain-containing proteins they named GRBs (for growth factor receptor (Montrer RYK Kits ELISA)-bound). They identified GRB-3 as having 77% identity at the protein level and 80% similarity at the DNA level to v-crk.
This gene encodes a member of an adapter protein family that binds to several tyrosine-phosphorylated proteins. The product of this gene has several SH2 and SH3 domains (src-homology domains) and is involved in several signaling pathways, recruiting cytoplasmic proteins in the vicinity of tyrosine kinase through SH2-phosphotyrosine interaction. The N-terminal SH2 domain of this protein functions as a positive regulator of transformation whereas the C-terminal SH3 domain functions as a negative regulator of transformation. Two alternative transcripts encoding different isoforms with distinct biological activity have been described.
, adapter molecule crk
, v-crk sarcoma virus CT10 oncogene homolog (avian)
, proto-oncogene c-Crk
, avian sarcoma virus CT10 (v-crk) oncogene homolog
, proto-oncogene C-crk
, v-crk sarcoma virus CT10 oncogene homolog
, SH2/SH3 adaptor Crk2
, SH2/SH3 adaptor crk
, CT-10 related kinase 3
, proto-oncogene c-crk
, v-crk sarcoma virus CT10 oncogene-like protein