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The adaptor proteins Crk (show CRK Proteins) and Crk (show CRK Proteins)-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, 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 (show SNAP29 Proteins), AIFM3 (show AIFM3 Proteins), and CRKL appear to be critical to the phenotype, with haploinsufficiency of CRKL emerging as the main genetic driver.
a role for miR (show MLXIP Proteins)-429 as a novel target suppressing invasion and migration of human cervical cancer cells through modulation of its targeting genes ZEB1 and CRKL, is reported.
CrkL mediates CCL20/CCR6-induced epithelial-to-mesenchymal transition via Akt pathway, instead of Erk1/2 pathway in development of gastric cancer
CrkL regulates CCL19 (show CCL19 Proteins) and CCR7 (show CCR7 Proteins)-induced epithelial-to-mesenchymal transition via ERK (show EPHB2 Proteins) signaling pathway in epithelial ovarian carcinoma patients.
these results suggest that CrkL plays a regulatory role in the SDF-1 (show CXCL12 Proteins)-induced Erk1/2 and PI3K (show PIK3CA Proteins)/Akt (show AKT1 Proteins) 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 Proteins) target miR (show MLXIP Proteins)-200b/200c/429 miRNAs are negative regulators of the CRKL oncogene (show RAB1A Proteins)
results suggested that overexpression of CRKL promoted cell invasion through upregulation of MMP9 (show MMP9 Proteins) expression and activation of ERK (show EPHB2 Proteins) pathway
results suggest that Crk (show CRK Proteins) 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 (show SORBS1 Proteins) and Sorbs2 (show Sorbs2 Proteins) 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 Proteins)/CRKL-deficient T cells resulted in efficient graft-versus-leukemia responses with minimal graft-versus-host disease in mice.
Crk1 (show MAPK14 Proteins)/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 Proteins) and CrkL have critical roles in cell structure and motility by maintaining cytoskeletal integrity.
The molecular signaling set off by ERalpha (show ESR1 Proteins) 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