KIAA1199 (KIAA1199) ELISA试剂盒

Human KIAA1199 interaction partners

1. study reveals that KIAA1199 promotes metastasis of colorectal cancer cells via microtubule destabilization regulated by a PP2A/stathmin pathway, and suggests that KIAA1199 may be a promising target for preventing metastasis in colorectal cancer.

2. Upregulation of CEMIP promotes migration and invasion in anoikis-resistant prostate cancer cells by enhancing PDK4-associated metabolic reprogramming.

3. expression of KIAA1199 is up-regulated in primary hepatocellular carcinoma, which is significantly correlated with the clinicopathological features and prognosis, high expression of KIAA1199 increased the risk of death in patients with primary hepatocellular carcinom

4. the in-vitro anti-proliferative and pro-apoptotic effects in colorectal cancer cells that were induced by silencing cell migration inducing hyaluronan binding protein may be associated with GRP78 repression and UPR attenuation

5. CEMIP expression was increased in retinoblastoma tissues and cells. miR-140-5p inhibited CEMIP expression possibly by targeting the 3'-UTR.

6. KIAA1199 is overexpressed in pancreatic intraepithelial neoplasia.

7. Our findings revealed that KIAA1199 protein could be applied in predicting nonsmall cell lung cancer patient's outcome

8. Overexpression of KIAA1199 may contribute to increased migration of pancreatic ductal adenocarcinoma cells and predict shorter survival after surgical resection.

9. Results suggest a possible link between inflammation, induced KIAA1199 expression, and enhanced migration during pancreatic ductal adenocarcinoma (PDAC) progression.

10. Elevated KIAA1199 protein expression is associated with tumor invasion and metastasis in colorectal cancer.

11. KIAA1199 promotes migration and invasion by Wnt/beta-catenin pathway and matrix metalloproteinase-mediated epithelial-mesenchymal transition progression, and serves as a poor prognosis marker in gastric cancer.

12. CEMIP directly facilitates colon tumor growth, and high CEMIP expression correlates with poor outcome in stage III and in stages II+III combined cohorts.

13. Results provide insight into the upregulation of CEMIP within cancer and can lead to novel treatment strategies targeting this cancer cell migration-promoting gene.

14. We present evidence that high expression of KIAA1199 is associated with tumor invasion depth, TNM stage, and poor prognosis in colorectal cancer

15. Regulation of Hyaluronan (HA) Metabolism Mediated by HYBID (Hyaluronan-binding Protein Involved in HA Depolymerization, KIAA1199) and HA Synthases in Growth Factor-stimulated Fibroblasts.

16. oncogenic protein induced by HPV infection and constitutive NF-kappaB activity that transmits pro-survival and invasive signals through EGFR signalling

17. KIAA1199 plays an important role in glycogen breakdown and cancer cell survival

18. KIAA1199 influences the proliferation, adhesion, motility, invasiveness and epithelial-to-mesenchymal transition of cancer cells, is a likely target gene of the Wnt/beta-catenin signalling pathway[review]

19. Findings indicate that KIAA1199 may play an important role in breast tumor growth and invasiveness.

20. proteins that might interact with KIAA1199 and molecular pathways in which it might play roles, were identified.

Mouse (Murine) KIAA1199 interaction partners

1. The KIAA1199, a protein that plays a role in a HA degradation pathway independent of the canonical hyaluronidases such as PH20, is specifically expressed in tissue lesions in which HA is degraded.

2. KIAA1199 is overexpressed in pancreatic intraepithelial neoplasia.

3. This work identifies KIAA1199 as a novel regulator of MEK/ERK-induced Schwann cell dedifferentiation and contributes to a better understanding of the molecular control of Schwann cell dedifferentiation.

4. Results indicate that HYaluronan Binding Protein Involved in hyaluronan Depolymerization (Hybid) plays a key role in memory function in the brain.