NDLI: The enormous influence of TNIK knockdown on intracellular signals and cell survival

Please wait, while we are loading the content...

The enormous influence of TNIK knockdown on intracellular signals and cell survival

Content Provider	Springer Nature Link
Author	Gui, Jinghua Yang, Baotian Wu, Jinyun Zhou, Xiumei
Copyright Year	2011
Abstract	Basic cellular activities and coordinated cell actions are governed by intracellular signals, among which the Wnt signaling cascade plays an important role in tissue polarity and cell adhesion or movement through the activation of c-Jun N-terminal kinase (JNK) pathway. As one of the central transcriptional factors, Traf2- and Nck-interacting kinase (TNIK) mediates the transactivation of Wnt target genes and promotes the activity of c-Jun N-terminus kinase (JNK)2 when overexpressed. To further understand the function of TNIK, changes in intracellular signals were detected in colon cancer cell lines using a knockdown strategy. In this study, we found that the short-hairpin RNA-mediated knockdown of TNIK decreased the expressions of CD44, c-MYC and cyclin D1, which was consistent with the results of a TCF-4 reporter assay. Our data showed, for the first time, that the activation of both JNK1 and JNK2 by TNFα could be blocked through TNIK knockdown, which dampened the AP1 luciferase activity accordingly. In addition, adenovirus mediated the downregulation of TNIK-triggered intrinsic apoptosis in SW480 cells by activating caspase-9 and PARP-1. We conclude that TNIK is essential for the activation of both the canonical Wnt pathway and the JNK pathway, and serves as a pro-survival factor.
Starting Page	121
Ending Page	126
Page Count	6
File Format	PDF
ISSN	09147470
Journal	Human Cell
Volume Number	24
Issue Number	3
e-ISSN	17490774
Language	English
Publisher	Springer Japan
Publisher Date	2011-06-28
Publisher Place	Japan
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Traf2 and NCK-interacting kinase Short-hairpin RNA Wnt c-Jun N-terminus kinase Apoptosis Stem Cells Embryology Cell Culture Oncology Cell Biology Reproductive Medicine
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Cancer Research

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Expression analysis of TRAF2‑ and NCK‑interacting protein kinase (TNIK) and phosphorylated TNIK in papillary thyroid carcinoma.

Dynamic change of TNIK in response to tumor necrosis factor alpha in a TRAF2-dependent manner

Traf2- and Nck-interacting Kinase Is Essential for Canonical Wnt Signaling in Xenopus Axis Formation

Feasibility of Targeting Traf2-and-Nck-Interacting Kinase in Synovial Sarcoma

Computational study on new natural compound inhibitors of Traf2 and Nck-interacting kinase (TNIK).

Epigenetic regulation of traf2- and Nck-interacting kinase (TNIK) in polycystic ovary syndrome.

Prognostic significance of Traf2- and Nck- interacting kinase (TNIK) in colorectal cancer

Deficiency of germinal center kinase TRAF2 and NCK-interacting kinase (TNIK) in B cells does not affect atherosclerosis

Traf2- and Nck-interacting kinase (TNIK) is involved in the anti-cancer mechanism of dovitinib in human multiple myeloma IM-9 cells

The enormous influence of TNIK knockdown on intracellular signals and cell survival

Similar Documents

Expression analysis of TRAF2‑ and NCK‑interacting protein kinase (TNIK) and phosphorylated TNIK in papillary thyroid carcinoma.

Dynamic change of TNIK in response to tumor necrosis factor alpha in a TRAF2-dependent manner

Traf2- and Nck-interacting Kinase Is Essential for Canonical Wnt Signaling in Xenopus Axis Formation

Feasibility of Targeting Traf2-and-Nck-Interacting Kinase in Synovial Sarcoma

Computational study on new natural compound inhibitors of Traf2 and Nck-interacting kinase (TNIK).

Epigenetic regulation of traf2- and Nck-interacting kinase (TNIK) in polycystic ovary syndrome.

Prognostic significance of Traf2- and Nck- interacting kinase (TNIK) in colorectal cancer

Deficiency of germinal center kinase TRAF2 and NCK-interacting kinase (TNIK) in B cells does not affect atherosclerosis

Traf2- and Nck-interacting kinase (TNIK) is involved in the anti-cancer mechanism of dovitinib in human multiple myeloma IM-9 cells

The enormous influence of TNIK knockdown on intracellular signals and cell survival