Doublecortin-Like Kinase 1 (DCLK1) ELISA Kits

Zebrafish Doublecortin-Like Kinase 1 (DCLK1) interaction partners

1. These results suggest that both the kinase domain and the Ser/Pro-rich domain are involved in regulating the microtubule-binding activity of doublecortin-like protein kinase (DCLK).

2. DCLK mediates its neuronal functions through phosphorylation of physiological substrates such as synapsin II

3. Gene knockdown studies of zDCLK suggest that zDCLK may play crucial roles in the central nervous systems during the early stage of embryogenesis.

Human Doublecortin-Like Kinase 1 (DCLK1) interaction partners

1. Let-7e plays an important role as tumor suppressor miRNA in colorectal cancer cells probably through inhibition of DCLK1 expression.

2. DCLK1 overexpression was significantly correlated with the stage of colorectal cancer (CRC), the presence of metastasis and poor survival rate. DCLK1 may be used to identify high-risk patients and those with chemotherapy-resistant tumors. [review]

3. Results provide evidence that DCLK1 labels a unique pancreatic cellular lineage in the intraductal papillary mucinous neoplasms (IPMN). The clustering of DCLK1(+) cells is an early event in Kras-induced pancreatic tumorigenesis and may contribute to IPMN initiation.

4. High alternative splice variants of DCLK1 mark cancer stem cells, promote self-renewal and drug-resistance in kidney cancer.

5. Investigations showed that DCLK1 induced the NF-kappaBp65 subunit expression through the PI3K/Akt/Sp1 axis and activated NF-kappaBp65 through the PI3K/Akt/IkappaBalpha pathway during the EMT of CRC cells. Findings identify DCLK1 as a pivotal regulator of an EMT axis in CRC.

6. DCLK1 plays an important role in cancer progression and is involved in the regulation of miR-200c expression.

7. The expression of DCLK1 was found in low-grade adenomas and increased with worsening severity of dysplasia. DCLK1 expression was highly observed in advanced adenomas, which had a clinically higher malignant potential.

8. Our findings indicated that the Lgr5High/DCLK1High expression pattern may be considered as a signature phenotype for intestinal subtypes of gastric carcinoma.

9. High DCLK1 expression is associated with malignant pleural mesothelioma.

10. On the basis of these data, FOXD3 is a potent repressor of DCLK1-S expression in normal cells; loss of FOXD3 in hCCCs/hCRCs allows upregulation of DCLK1-S, imparting a potent invasive potential to the cells

11. Expression levels of phosphorylated cdc25A (p-cdc25A) and phosphorylated Chk1 (p-Chk1), belonging to the ATR pathway, were decreased by treatment with Dclk1 inhibitor LRRK2-IN-1 (LRRK), indicating Dclk1 involvement in the ATR pathway

12. In rectal cancer patients treated with preoperative chemoradiotherapy (CRT), DCLK1 expression was significantly correlated with lymph node metastasis and poor cancer-specific survival. However, in patients treated without preoperative therapy, no such correlation was found. DCLK1 expression can be associated with lymph node metastasis and poor cancer-specific survival in rectal cancer patients who receive CRT.

13. Pancreatic ductal adenocarcinoma patients with DCLK1-positive tumors had significantly shorter survival times than those with DCLK1-negative tumors.

14. DCLK1 plays crucial role in the regulation of epithelial-mesenchymal transition.DCLK1 is highly expressed in pancreatic neuroendocrine tumor.

15. DCLK1 is a prognostic biomarker for shortened survival. Secondly, through inhibition of DCLK1, it may serve as a therapeutic target as well

16. DCLK1 has been identified as a potential target for miR-448 to regulate lung squamous cell carcinoma cells growth.

17. 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.

18. 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

19. Biochemical and structural characterization of DCLK1 allowed for the mapping of cancer-causing mutations within the kinase domain.

20. Hence, we outline and discuss emerging evidence that strongly supports tuft cells as key regulatory cells in the complex network of the intestinal microenvironment. [review]

Mouse (Murine) Doublecortin-Like Kinase 1 (DCLK1) interaction partners

1. High alternative splice variants of DCLK1 mark cancer stem cells, promote self-renewal and drug-resistance in kidney cancer.

2. intestinal tuft cells play an important role in regulating the ATM mediated DNA damage response, for epithelial cell survival/self-renewal via a Dclk1 dependent mechanism

3. Dclk1 contributes functionally to the pathogenesis of pancreatic cancer; Dclk1 marks quiescent pancreatic progenitors that are candidates for the origin of pancreatic cancer

4. loss of parietal cells leads to the reversible emergence of a novel Dclk1-expressing sensory cell population in the gastric mucosa.

5. Dclk1 plays an important role in regulating colonic inflammatory response and colonic epithelial integrity

6. Dclk1 promotes axonal regeneration, neuronal survival, and growth core reformation via microtubule stabilization, prevention of F-actin destabilization and synergy with mTOR.

7. Dclk1 is critically involved in facilitating intestinal tumorigenesis by enhancing pluripotency and EMT factors in Apc mutant intestinal tumors and it also provides a potential therapeutic target for the treatment of colorectal cancer.

8. Dclk1 plays a functional role critical in the epithelial restorative response.

9. DCLK1 regulates pluripotency and angiogenic factors via microRNA-dependent mechanisms in pancreatic cancer.

10. 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.

11. Pancreatic neoplasms in mice contain morphologically and functionally distinct subpopulations, expressing DCLK1, that have cancer stem cell-like properties.

12. DCAMKL1 represses osteoblast activation by antagonizing Runx2, the master transcription factor in osteoblasts.

13. Doublecortin-like kinases are critical regulators of dendritic development by means of their specific targeting to the distal dendrites, and their local control of dendritic growth and synapse maturation.

14. The neurons lacking Dcx and/or its structurally conserved paralogue, doublecortin-like kinase 1 (Dclk1), show impaired Kif1a-mediated transport of Vamp2, a cargo of Kif1a, with decreased run length.

15. Our findings define DCL as a novel marker for specific aspects of adult neurogenesis, which partly overlap with doublecortin

16. Gastric tuft cells express DCLK1 and are expanded in hyperplasia

17. A truncated, constitutively active form of DCLK-short is highly expressed in the hippocampus, cortex and amygdala of transgenic mice. These mice spend less time, move less in the open arms of the maze and show a reduction in the number of rim dips.

18. The DCLK gene product affects glutamatergic neuronal transmission in response to neurological stimuli.

19. genomic organization underlying the splice variants of DCLK and the expression profile of two splice variants affecting the kinase domain of DCLK and CPG16 (candidate plasticity gene 16).

20. DCLK controls mitotic division by regulating spindle formation and also determines the fate of neural progenitors during cortical neurogenesis.