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Items: 1 to 20 of 88

1.

The p16(INK4A) tumor suppressor regulates cellular oxidative stress.

Jenkins NC, Liu T, Cassidy P, Leachman SA, Boucher KM, Goodson AG, Samadashwily G, Grossman D.

Oncogene. 2011 Jan 20;30(3):265-74. doi: 10.1038/onc.2010.419.

2.

Familial melanoma-associated mutations in p16 uncouple its tumor-suppressor functions.

Jenkins NC, Jung J, Liu T, Wilde M, Holmen SL, Grossman D.

J Invest Dermatol. 2013 Apr;133(4):1043-51. doi: 10.1038/jid.2012.401.

3.

Role of melanin in melanocyte dysregulation of reactive oxygen species.

Jenkins NC, Grossman D.

Biomed Res Int. 2013;2013:908797. doi: 10.1155/2013/908797.

4.

Reactive oxygen species promotes cellular senescence in normal human epidermal keratinocytes through epigenetic regulation of p16(INK4a.).

Sasaki M, Kajiya H, Ozeki S, Okabe K, Ikebe T.

Biochem Biophys Res Commun. 2014 Sep 26;452(3):622-8. doi: 10.1016/j.bbrc.2014.08.123.

PMID:
25181340
6.
7.

Tumor suppressor genes and ROS: complex networks of interactions.

Vurusaner B, Poli G, Basaga H.

Free Radic Biol Med. 2012 Jan 1;52(1):7-18. doi: 10.1016/j.freeradbiomed.2011.09.035. Review.

PMID:
22019631
8.

Hepatitis B virus X protein overcomes stress-induced premature senescence by repressing p16(INK4a) expression via DNA methylation.

Kim YJ, Jung JK, Lee SY, Jang KL.

Cancer Lett. 2010 Feb 28;288(2):226-35. doi: 10.1016/j.canlet.2009.07.007.

PMID:
19656618
9.

Absence of AMPKα2 accelerates cellular senescence via p16 induction in mouse embryonic fibroblasts.

Ding Y, Chen J, Okon IS, Zou MH, Song P.

Int J Biochem Cell Biol. 2016 Feb;71:72-80. doi: 10.1016/j.biocel.2015.12.010.

PMID:
26718972
10.

Oxidative stress and premature senescence in corneal endothelium following penetrating keratoplasty in an animal model.

Zhao X, Wang Y, Wang Y, Li S, Chen P.

BMC Ophthalmol. 2016 Feb 2;16:16. doi: 10.1186/s12886-016-0192-6.

11.

The physiology of p16(INK4A)-mediated G1 proliferative arrest.

Shapiro GI, Edwards CD, Rollins BJ.

Cell Biochem Biophys. 2000;33(2):189-97. Review.

PMID:
11325039
12.

Progression of genotype-specific oral cancer leads to senescence of cancer-associated fibroblasts and is mediated by oxidative stress and TGF-β.

Hassona Y, Cirillo N, Lim KP, Herman A, Mellone M, Thomas GJ, Pitiyage GN, Parkinson EK, Prime SS.

Carcinogenesis. 2013 Jun;34(6):1286-95. doi: 10.1093/carcin/bgt035.

14.

The atr protein kinase controls UV-dependent upregulation of p16INK4A through inhibition of Skp2-related polyubiquitination/degradation.

Al-Khalaf HH, Hendrayani SF, Aboussekhra A.

Mol Cancer Res. 2011 Mar;9(3):311-9. doi: 10.1158/1541-7786.MCR-10-0506.

15.

Functional analysis of wild-type and malignant glioma derived CDKN2Abeta alleles: evidence for an RB-independent growth suppressive pathway.

Arap W, Knudsen E, Sewell DA, Sidransky D, Wang JY, Huang HJ, Cavenee WK.

Oncogene. 1997 Oct 23;15(17):2013-20.

16.

Depletion of ERK2 but not ERK1 abrogates oncogenic Ras-induced senescence.

Shin J, Yang J, Lee JC, Baek KH.

Cell Signal. 2013 Dec;25(12):2540-7. doi: 10.1016/j.cellsig.2013.08.014.

PMID:
23993963
17.

p16(Ink4a) in melanocyte senescence and differentiation.

Sviderskaya EV, Hill SP, Evans-Whipp TJ, Chin L, Orlow SJ, Easty DJ, Cheong SC, Beach D, DePinho RA, Bennett DC.

J Natl Cancer Inst. 2002 Mar 20;94(6):446-54. Erratum in: J Natl Cancer Inst 2002 Jun 5;94(11):866.

18.

Loss of p16Ink4a confers susceptibility to metastatic melanoma in mice.

Krimpenfort P, Quon KC, Mooi WJ, Loonstra A, Berns A.

Nature. 2001 Sep 6;413(6851):83-6.

PMID:
11544530
19.

Hypertension induces somatic cellular senescence in rats and humans by induction of cell cycle inhibitor p16INK4a.

Westhoff JH, Hilgers KF, Steinbach MP, Hartner A, Klanke B, Amann K, Melk A.

Hypertension. 2008 Jul;52(1):123-9. doi: 10.1161/HYPERTENSIONAHA.107.099432.

20.

Predicting functional significance of cancer-associated p16(INK4a) mutations in CDKN2A.

McKenzie HA, Fung C, Becker TM, Irvine M, Mann GJ, Kefford RF, Rizos H.

Hum Mutat. 2010 Jun;31(6):692-701. doi: 10.1002/humu.21245.

PMID:
20340136
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