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DCLK1 encodes a member of the protein kinase superfamily and the doublecortin family. Additionally we are shipping DCLK1 Antibodies (113) and DCLK1 Proteins (15) and many more products for this protein.
Showing 8 out of 20 products:
Mouse (Murine) DCLK1 ELISA Kit for Sandwich ELISA - ABIN428382
Qu, Johnson, Chandrakesan, Weygant, May, Aiello, Rhim, Zhao, Zheng, Lightfoot, Pant, Irvan, Postier, Hocker, Hanas, Ali, Sureban, An, Schlosser, Stanger, Houchen: Doublecortin-like kinase 1 is elevated serologically in pancreatic ductal adenocarcinoma and widely expressed on circulating tumor cells. in PLoS ONE 2015
These results suggest that both the kinase domain and the Ser (show SIGLEC1 ELISA Kits)/Pro-rich domain are involved in regulating the microtubule-binding activity of doublecortin (show DCX ELISA Kits)-like protein kinase (show TGFB3 ELISA Kits) (DCLK (show DCLK2 ELISA Kits)).
DCLK (show DCLK2 ELISA Kits) mediates its neuronal functions through phosphorylation of physiological substrates such as synapsin II (show SYN2 ELISA Kits)
Gene knockdown studies of zDCLK (show DCLK2 ELISA Kits) suggest that zDCLK (show DCLK2 ELISA Kits) may play crucial roles in the central nervous systems during the early stage of embryogenesis.
DCLK1 up-regulation may play a contributory role in colorectal cancer metastasis and poor prognosis via activation of EMT (show ITK ELISA Kits). DCLK1 may serve as an independent predictor for CRC (show CALR ELISA Kits) prognosis.
Results showed the mechanism in which miR (show MLXIP ELISA Kits)-137 regulates the expression of DCLK1, and demonstrated the opposite expression patterns of miR (show MLXIP ELISA Kits)-137/DCLK1 in human non-small cell lung carcinoma and colon cancer stem cells.
DCLK1 promoter methylationis associated with lung cancer.
DCLK1 expression could aid in the prognostication and management of breast cancer with neuroendocrine differentiation.
DCLK1 controls these complex cellular signaling pathways to regulate hepatocellular carcinoma growth, and may be used as a prognostic biomarker.
results provide new insights into the molecular mechanism of the hepatitis B/C-virus induced liver inflammation and tumorigenesis via DCLK1-controlled networks
Data suggest that doublecortin and CaM kinase-like 1 protein short-transcripts (DCLK1-S) may represent an important target for preventing/inhibiting colon-cancers, and for eliminating colon-cancer-stem-cells (CSCs).
DCLK1 is essential for the invasive and metastatic properties of pancreatic cancer stem cells.
Data indicate that doublecortin-like kinase 1 (DCLK1) is overexpressed and has a unique methylation signature in renal clear cell carcinoma (RCC (show XRCC1 ELISA Kits)).
Doublecortin-like kinase 1 is elevated serologically in pancreatic ductal adenocarcinoma and widely expressed on circulating tumor cells.
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 ELISA Kits).
Dclk1 is critically involved in facilitating intestinal tumorigenesis by enhancing pluripotency and EMT (show ITK ELISA Kits) factors in Apc (show APC ELISA Kits) 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 ELISA Kits), 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