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抗Human CrkL 抗体:
抗Rat (Rattus) CrkL 抗体:
抗Mouse (Murine) CrkL 抗体:
Human Monoclonal CrkL Primary Antibody for ICS - ABIN1177226
Arai, Nosaka, Kohsaka, Miyasaka, Miura: CrkL activates integrin-mediated hematopoietic cell adhesion through the guanine nucleotide exchange factor C3G. in Blood 1999
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Human Monoclonal CrkL Primary Antibody for ICS - ABIN1177227
Feller: Crk family adaptors-signalling complex formation and biological roles. in Oncogene 2001
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Human Monoclonal CrkL Primary Antibody for ICS - ABIN1177228
Senechal, Heaney, Druker, Sawyers: Structural requirements for function of the Crkl adapter protein in fibroblasts and hematopoietic cells. in Molecular and cellular biology 1998
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Human Monoclonal CrkL Primary Antibody for IF, PLA - ABIN514606
Segovis, Schoon, Dick, Nacusi, Leibson, Billadeau: PI3K links NKG2D signaling to a CrkL pathway involved in natural killer cell adhesion, polarity, and granule secretion. in Journal of immunology (Baltimore, Md. : 1950) 2009
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Human Monoclonal CrkL Primary Antibody for FACS, ELISA - ABIN969064
Seo, Suenaga, Hatakeyama, Taiji, Imamoto: Structural and functional basis of a role for CRKL in a fibroblast growth factor 8-induced feed-forward loop. in Molecular and cellular biology 2009
Human Monoclonal CrkL Primary Antibody for FACS, ELISA - ABIN965932
Sowa, Bennett, Gygi, Harper: Defining the human deubiquitinating enzyme interaction landscape. in Cell 2009
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Human Polyclonal CrkL Primary Antibody for ELISA, WB - ABIN546773
Singer, Hudelist, Lamm, Mueller, Handl, Kubista, Czerwenka: Active (p)CrkL is overexpressed in human malignancies: potential role as a surrogate parameter for therapeutic tyrosine kinase inhibition. in Oncology reports 2006
Human Polyclonal CrkL Primary Antibody for IF, PLA - ABIN514605
Liu, Chen, Chau, Jan, Chen, Hsu, Lin, Juang, Lu, Cheng, Chen, Chang, Ting, Kao, Hsiao, Huang: Analysis of protein-protein interactions in cross-talk pathways reveals CRKL protein as a novel prognostic marker in hepatocellular carcinoma. in Molecular & cellular proteomics : MCP 2013
The adaptor proteins Crk and Crk-like (Crkl), with which Dock proteins are known to interact physically, are also required for myoblast fusion.
Taken together, our data demonstrated that miR-429 might function as an antimetastatic miRNA to regulate HCC metastasis by directly targeting CRKL via modulating Raf/MEK/ERK-epithelial mesenchymal transition pathway.
High CRKL expression is associated with Cervical Cancer.
Silencing CRKL expression in PTEN-null human cancer cells leads to a decrease in p110beta-dependent PI3K signaling and cell proliferation.
Study found the expression of CRKL up-regulated and correlated with that of ABCG2 in gastric neoplasm. CRKL is one of the downstream molecules regulated by ABCG2, which promotes cell growth.
We demonstrated that CRKL is a novel downstream effector of ALK signaling in non-small-cell lung cancer
Dynamic multi-site phosphorylation by Fyn and Abl drives the interaction between CRKL and the novel scaffolding receptors DCBLD1 and DCBLD2.
Data show that miR-193b, by directly targeting focal adhesion kinase (FAK), CRK-like proto-oncogene (CRKL), and methionine sulfoxide reductase A (MSRA), regulates focal adhesion signaling and ROS signaling, which play pivotal roles in liposarcomagenesis and adipogenic differentiation.
TP53-miR-215-PCAT-1-CRKL axis might represent an important regulatory pathway in hepatocellular carcinoma.
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, AIFM3, and CRKL appear to be critical to the phenotype, with haploinsufficiency of CRKL emerging as the main genetic driver.
a role for miR-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 and CCR7-induced epithelial-to-mesenchymal transition via ERK signaling pathway in epithelial ovarian carcinoma patients.
these results suggest that CrkL plays a regulatory role in the SDF-1-induced Erk1/2 and PI3K/Akt 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 target miR-200b/200c/429 miRNAs are negative regulators of the CRKL oncogene
results suggested that overexpression of CRKL promoted cell invasion through upregulation of MMP9 expression and activation of ERK pathway
CRKL has the potential to be used as a biomarker for the diagnosis, treatment and prognosis of certain tumors
We identified ZEB1 and CRKL as potential targets of miR-429 by analyzing combined results from in silico search and global expression array of the same RNA samples. Immunoblot assay confirmed that miR-429 reduced their expression at protein level.
results suggest that Crk 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 and Sorbs2 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/CRKL-deficient T cells resulted in efficient graft-versus-leukemia responses with minimal graft-versus-host disease in mice.
Crk1/2 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 and CrkL have critical roles in cell structure and motility by maintaining cytoskeletal integrity.
The molecular signaling set off by ERalpha 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
Data show a critical role for Crk and Crk-L downstream from Dok-7 in presynaptic and postsynaptic differentiation.
a BCR-ABL mutant lacking direct binding sites for the GRB2, CBL and CRKL adapter proteins fails to induce leukemia in mice
CrkL plays a specific role in integrin-induced migration as a downstream mediator of Src.
CrkL is not absolutely required for T cell development or function.
These results suggest a role for CrkL in the Reelin signaling pathway to control neuronal migration.
The Crk family proteins are important downstream components of the reelin signaling pathway in the regulation of postnatal hippocampal dendritogenesis.
Crk and CrkL play essential overlapping functions in the Reelin signaling pathway.
Crkol is essential for cranial and cardiac neural crest development. The chromosomal location of the human CRKL gene (22q11.21) and the phenotype of Crkol mutant mice suggest that defects in CRKL-mediated pathways underlie DiGeorge syndrome.
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