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DCLK1 encodes a member of the protein kinase superfamily and the doublecortin family. Additionally we are shipping DCLK1 Antibodies (116) and DCLK1 Kits (24) and many more products for this protein.
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These results suggest that both the kinase domain and the Ser (show SIGLEC1 Proteins)/Pro-rich domain are involved in regulating the microtubule-binding activity of doublecortin (show DCX Proteins)-like protein kinase (show TGFB3 Proteins) (DCLK (show DCLK2 Proteins)).
DCLK (show DCLK2 Proteins) mediates its neuronal functions through phosphorylation of physiological substrates such as synapsin II (show SYN2 Proteins)
Gene knockdown studies of zDCLK (show DCLK2 Proteins) suggest that zDCLK (show DCLK2 Proteins) may play crucial roles in the central nervous systems during the early stage of embryogenesis.
Generated a (doublecortin like kinase 1) DCLK1-S-specific polyclonal antibody (S-isoform specific), and studied its use in screening of colon cancer after colonoscopy.
DCLK1 expression was observed in tumor cells in patients with pathological stage I non-small cell lung cancer (NSCLC)and was correlated with adverse prognosis, especially in patients with adenocarcinoma. DCLK1 may be a potential new therapeutic target
Biochemical and structural characterization of DCLK1 allowed for the mapping of cancer-causing mutations within the kinase domain.
Our results indicate that Dclk1 is essential in advancing intestinal tumorigenesis. Knocking down Dclk1 decreases tumor stemness and progression and is thus predicted to regulate pro-survival signaling and tumor cell pluripotency.
The univariate and multivariate analyses suggested DCAMKL1 protein overexpression was an unfavorable prognostic factor in bladder cancer patients. In conclusion, DCAMKL1 is an independent poor prognostic factor for bladder cancer patients.
DCLK1 induction and its overexpression following hepatic injury are likely to contribute to tumorigenesis including maintenance and dissemination of tumor cells in circulation.
first evidence for the suppressive activity of miR (show MLXIP Proteins)-613 in hepatocellular carcinoma, which is causally linked to targeting of DCLK1
MSX1 (show MSX1 Proteins) and DCLK1 might be used in colorectal cancer detection or as target of cancer therapies.
Increased expression of stromal DCLK1 was detected in endometriotic tissue compared to endometriosis patient endometrium. Stromal expression of DCLK1 was increased in endometrium of endometriosis patients compared to controls.
DCLK1 up-regulation may play a contributory role in colorectal cancer metastasis and poor prognosis via activation of EMT (show ITK Proteins). DCLK1 may serve as an independent predictor for CRC (show CALR Proteins) prognosis.
Dclk1 contributes functionally to the pathogenesis of pancreatic cancer; Dclk1 marks quiescent pancreatic progenitors that are candidates for the origin of pancreatic cancer
loss of parietal cells leads to the reversible emergence of a novel Dclk1-expressing sensory cell population in the gastric mucosa.
Dclk1 plays an important role in regulating colonic inflammatory response and colonic epithelial integrity
Dclk1 promotes axonal regeneration, neuronal survival, and growth core reformation via microtubule stabilization, prevention of F-actin destabilization and synergy with mTOR (show FRAP1 Proteins).
Dclk1 is critically involved in facilitating intestinal tumorigenesis by enhancing pluripotency and EMT (show ITK Proteins) factors in Apc (show APC Proteins) mutant intestinal tumors and it also provides a potential therapeutic target for the treatment of colorectal cancer.
Dclk1 plays a functional role critical in the epithelial restorative response.
DCLK1 regulates pluripotency and angiogenic factors via microRNA-dependent mechanisms in pancreatic cancer.
These results suggest that crypt epithelial cell Dclk1 expression can be used as one potential marker to evaluate the early survival of intestinal stem cells following severe radiation injury.
Pancreatic neoplasms in mice contain morphologically and functionally distinct subpopulations, expressing DCLK1, that have cancer stem cell-like properties.
DCAMKL1 represses osteoblast activation by antagonizing Runx2 (show RUNX2 Proteins), the master transcription factor in osteoblasts.
This gene encodes a member of the protein kinase superfamily and the doublecortin family. The protein encoded by this gene contains two N-terminal doublecortin domains, which bind microtubules and regulate microtubule polymerization, a C-terminal serine/threonine protein kinase domain, which shows substantial homology to Ca2+/calmodulin-dependent protein kinase, and a serine/proline-rich domain in between the doublecortin and the protein kinase domains, which mediates multiple protein-protein interactions. The microtubule-polymerizing activity of the encoded protein is independent of its protein kinase activity. The encoded protein is involved in several different cellular processes, including neuronal migration, retrograde transport, neuronal apoptosis and neurogenesis. This gene is up-regulated by brain-derived neurotrophic factor and associated with memory and general cognitive abilities. Multiple transcript variants generated by two alternative promoter usage and alternative splicing have been reported, but the full-length nature and biological validity of some variants have not been defined. These variants encode different isoforms, which are differentially expressed and have different kinase activities.
doublecortin-like kinase 1
, doublecortin and CaM kinase-like 1
, doublecortin and calcium/calmodulin-dependent protein kinase-like 1
, serine/threonine-protein kinase DCLK1
, doublecortin-like kinase 2
, serine/threonine-protein kinase DCLK1-like
, doublecortin domain-containing protein 3A
, doublecortin-like and CAM kinase-like 1
, CLICK-I beta
, double cortin and calcium/calmodulin-dependent protein kinase-like 1