PMID: 11323223Apr 27, 2001Paper

Abnormal NF-kappaB signaling pathway with enhanced susceptibility to apoptosis in immortalized keratinocytes

Journal of Dermatological Science
V ChaturvediB J Nickoloff

Abstract

The transcriptional activation and proper regulation of NF-kappaB is known to be important to the apoptotic resistant phenotype of epidermal-derived keratinocytes. By comparing and contrasting the responses of normal foreskin-derived keratinocytes versus an immortalized skin-derived keratinocyte cell line (i.e. HaCaT cells), several molecular defects involving NF-kappaB signaling pathway were delineated in the immortalized keratinocytes. While exposure to IFN-gamma plus TPA produces growth arrest in both normal and immortalized keratinocytes, with rapid phosphorylation of MEKKI and recruitment of distinctive protein kinase C isoforms into the signalosome complex, subsequent molecular events necessary for NF-kappaB activation were abnormal in HaCaT cells. This disrupted NF-kappaB activation in HaCaT cells was accompanied by enhanced susceptibility to UV-light induced apoptosis, which was associated with elevated levels of E2F-1 and decreased TRAF1/TRAF2 levels. Additional defects in HaCaT cells included markedly diminished levels of IKKbeta (and lack of induction of kinase activity) in response to inflammatory stimuli, a failure of p21(WAF1/CIP1) to associate with CDK2, and a decreased association between p65 and p300. These stu...Continue Reading

References

Mar 1, 1988·The Journal of Cell Biology·P BoukampN E Fusenig
Jun 6, 1995·Proceedings of the National Academy of Sciences of the United States of America·C MisseroG P Dotto
Feb 1, 1993·Experimental Dermatology·R PausB M Czarnetzki
Apr 1, 1997·Proceedings of the National Academy of Sciences of the United States of America·M E GerritsenT Collins
Apr 16, 1998·Proceedings of the National Academy of Sciences of the United States of America·C S SeitzP A Khavari
Aug 26, 1998·Biochemical Pharmacology·A W Snowden, N D Perkins
Apr 9, 1999·Science·K TakedaS Akira
Jul 14, 1999·The American Journal of Surgical Pathology·T Brink, J O Gebbers
Aug 7, 1999·The Journal of Biological Chemistry·V ChaturvediB J Nickoloff
Sep 17, 1999·The Journal of Biological Chemistry·M Karin
Dec 23, 1999·The Journal of Biological Chemistry·J Z QinB J Nickoloff
Jan 5, 2000·Molecular Cell·A C PhillipsK H Vousden
Jun 1, 2000·The Journal of Cell Biology·C K Kaufman, E Fuchs
May 16, 2006·Journal of Cutaneous Medicine and Surgery·Jeffrey Chow, Victor A Tron

❮ Previous
Next ❯

Citations

Jan 27, 2007·Archives of Dermatological Research·Davina A Lewis, Dan F Spandau
Jul 14, 2011·Archives of Dermatological Research·Lilla BariMárta Széll
Sep 28, 2013·Archives of Dermatological Research·Visalini Muthusamy, Terrence J Piva
Jan 10, 2003·The Journal of Investigative Dermatology. Symposium Proceedings·Brian J NickoloffMitchell F Denning
Apr 13, 2007·Radiation and Environmental Biophysics·Christine E Hellweg, Christa Baumstark-Khan
Jun 3, 2006·The Journal of Investigative Dermatology·Davina A LewisDan F Spandau
Dec 7, 2007·The Journal of Investigative Dermatology·Davina A Lewis, Dan F Spandau
Nov 11, 2005·The British Journal of Dermatology·S YokoyamaG Takahashi
Jan 19, 2006·The Journal of Investigative Dermatology·Deepak RajDouglas Grossman
Aug 4, 2009·Experimental Dermatology·Ilse S DaehnTimothy E Rayner
Dec 16, 2006·The Journal of Biological Chemistry·Sarah A BoswellSam W Lee
Aug 25, 2005·The Journal of Investigative Dermatology·Mayumi KomineKunihiko Tamaki

❮ Previous
Next ❯

Related Concepts

Related Feeds

Cell Checkpoints & Regulators

Cell cycle checkpoints are a series of complex checkpoint mechanisms that detect DNA abnormalities and ensure that DNA replication and repair are complete before cell division. They are primarily regulated by cyclins, cyclin-dependent kinases, and the anaphase-promoting complex/cyclosome. Here is the latest research.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis