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The adaptor proteins Crk (show CRK ELISA Kits) and Crk (show CRK ELISA Kits)-like (Crkl), with which Dock proteins are known to interact physically, are also required for myoblast fusion.
CrkL mediates CCL20 (show CCL20 ELISA Kits)/CCR6 (show CCR6 ELISA Kits)-induced epithelial-to-mesenchymal transition via Akt (show AKT1 ELISA Kits) pathway, instead of Erk1/2 (show MAPK1/3 ELISA Kits) pathway in development of gastric cancer
CrkL regulates CCL19 (show CCL19 ELISA Kits) and CCR7 (show CCR7 ELISA Kits)-induced epithelial-to-mesenchymal transition via ERK (show EPHB2 ELISA Kits) signaling pathway in epithelial ovarian carcinoma patients.
these results suggest that CrkL plays a regulatory role in the SDF-1 (show CXCL12 ELISA Kits)-induced Erk1/2 (show MAPK1/3 ELISA Kits) and PI3K (show PIK3CA ELISA Kits)/Akt (show 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 (show TP53 ELISA Kits) target miR (show MLXIP ELISA Kits)-200b/200c/429 miRNAs are negative regulators of the CRKL oncogene (show RAB1A ELISA Kits)
results suggested that overexpression of CRKL promoted cell invasion through upregulation of MMP9 (show MMP9 ELISA Kits) expression and activation of ERK (show EPHB2 ELISA Kits) pathway
CRKL has the potential to be used as a biomarker for the diagnosis, treatment and prognosis of certain tumors
We identified ZEB1 (show ZEB1 ELISA Kits) and CRKL as potential targets of miR (show MLXIP ELISA Kits)-429 by analyzing combined results from in silico search and global expression array of the same RNA samples. Immunoblot assay confirmed that miR (show MLXIP ELISA Kits)-429 reduced their expression at protein level.
These results indicate that CRKL gene amplification is rare in acquisition of resistance to EGFR (show EGFR ELISA Kits)-TKIs in lung cancer patients with EGFR (show EGFR ELISA Kits) mutations.
CrkL knockdown markedly suppressed the phosphorylated ERK (show EPHB2 ELISA Kits) (p-ERK (show EPHB2 ELISA Kits)) as well as the phosphorylated AKT (p-AKT (show AKT1 ELISA Kits)) (p < 0.001) compared with control or TGF-b1 alone.
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 (show SORBS1 ELISA Kits) and Sorbs2 (show 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 (show CRK ELISA Kits)/CRKL-deficient T cells resulted in efficient graft-versus-leukemia responses with minimal graft-versus-host disease in mice.
Crk1 (show 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 (show CRK ELISA Kits) and CrkL have critical roles in cell structure and motility by maintaining cytoskeletal integrity.
The molecular signaling set off by ERalpha (show ESR1 ELISA Kits) and CrkL association may have a central role in pregnancy and cancer.
Reelin-induced Dab1 tyrosine phosphorylation may generate a multifaceted signaling scaffold containing a rich array of Crk/CrkL-SH3 binding effectors
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