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The adaptor proteins Crk (zeige CRK ELISA Kits) and Crk (zeige CRK ELISA Kits)-like (Crkl), with which Dock proteins are known to interact physically, are also required for myoblast fusion.
The impaired T-cell proliferation and reduction of CRKL, phosphorylated CRKL, and c-Fos levels suggest a possible role of CRKL in functional deficiencies of T cells in patients with pDGS.
he findings in this study indicate a regulation relationship between CRKL and SLC7A5 (zeige SLC7A5 ELISA Kits), and provide useful evidence for gastric cancer therapeutic strategies.
We identified a recurrent 370-kb deletion at the 22q11.2 locus as a driver of kidney defects in the DiGeorge syndrome and in sporadic congenital kidney and urinary tract anomalies. SNAP29 (zeige SNAP29 ELISA Kits), AIFM3 (zeige AIFM3 ELISA Kits), and CRKL appear to be critical to the phenotype, with haploinsufficiency of CRKL emerging as the main genetic driver.
a role for miR (zeige MLXIP ELISA Kits)-429 as a novel target suppressing invasion and migration of human cervical cancer cells through modulation of its targeting genes ZEB1 (zeige ZEB1 ELISA Kits) and CRKL, is reported.
CrkL mediates CCL20 (zeige CCL20 ELISA Kits)/CCR6 (zeige CCR6 ELISA Kits)-induced epithelial-to-mesenchymal transition via Akt (zeige AKT1 ELISA Kits) pathway, instead of Erk1/2 (zeige MAPK1/3 ELISA Kits) pathway in development of gastric cancer
CrkL regulates CCL19 (zeige CCL19 ELISA Kits) and CCR7 (zeige CCR7 ELISA Kits)-induced epithelial-to-mesenchymal transition via ERK (zeige EPHB2 ELISA Kits) signaling pathway in epithelial ovarian carcinoma patients.
these results suggest that CrkL plays a regulatory role in the SDF-1 (zeige CXCL12 ELISA Kits)-induced Erk1/2 (zeige MAPK1/3 ELISA Kits) and PI3K (zeige PIK3CA ELISA Kits)/Akt (zeige AKT1 ELISA Kits) pathways and further managed the invasion and migration of breast cancer cells
The authors show that this potentiation involves reorganization of the natural CrkL-p85beta complex into a novel trimeric complex where influenza A virus NS1 serves as a bridging factor.
Our results demonstrate that the p53 (zeige TP53 ELISA Kits) target miR (zeige MLXIP ELISA Kits)-200b/200c/429 miRNAs are negative regulators of the CRKL oncogene (zeige RAB1A ELISA Kits)
results suggested that overexpression of CRKL promoted cell invasion through upregulation of MMP9 (zeige MMP9 ELISA Kits) expression and activation of ERK (zeige EPHB2 ELISA Kits) pathway
results suggest that Crk (zeige CRK ELISA Kits) and CrkL 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.
The study screened CrkL binding proteins using RNA interference (RNAi) and identified Sorbs1 (zeige SORBS1 ELISA Kits) and Sorbs2 (zeige Sorbs2 ELISA Kits) as two proteins that are enriched at AChR clusters and are required for the formation of AChR aggregation in vitro.
CRKL plays an important role in hepatocarcinoma cell proliferation, invasion and migration as well hepatocarcinoma malignancy and metastasis.
CRKL is shown to act as a potential suppressor and to provide new insight for both the malignant behaviors of hepatocarcinoma cells and lymphatic metastasis mechanism of hepatocarcinoma.
Sprouty2 acts as an inhibitor of CrkL-Rap1 signaling.
Differential migration of CRK (zeige CRK ELISA Kits)/CRKL-deficient T cells resulted in efficient graft-versus-leukemia responses with minimal graft-versus-host disease in mice.
Crk1 (zeige MAPK14 ELISA Kits)/2 and CrkL are physically linked, functionally complement each other during podocyte foot process spreading, and together are required for developing typical foot process architecture.
Results suggest that Crk (zeige CRK ELISA Kits) and CrkL have critical roles in cell structure and motility by maintaining cytoskeletal integrity.
The molecular signaling set off by ERalpha (zeige ESR1 ELISA Kits) and CrkL association may have a central role in pregnancy and cancer.
This gene encodes a protein kinase containing SH2 and SH3 (src homology) domains which has been shown to activate the RAS and JUN kinase signaling pathways and transform fibroblasts in a RAS-dependent fashion. It is a substrate of the BCR-ABL tyrosine kinase, plays a role in fibroblast transformation by BCR-ABL, and may be oncogenic.
v-crk sarcoma virus CT10 oncogene homolog (avian)-like
, crk-like protein
, v-crk sarcoma virus CT10 oncogene homolog-like
, v-crk avian sarcoma virus CT10 oncogene homolog-like