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Koji Itahana

Researcher at National University of Singapore

Publications -  59
Citations -  10440

Koji Itahana is an academic researcher from National University of Singapore. The author has contributed to research in topics: Senescence & Cancer. The author has an hindex of 27, co-authored 56 publications receiving 9580 citations. Previous affiliations of Koji Itahana include University of Texas MD Anderson Cancer Center & University of North Carolina at Chapel Hill.

Papers
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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Tumor suppressor ARF degrades B23, a nucleolar protein involved in ribosome biogenesis and cell proliferation.

Koji Itahana, +6 more
- 01 Nov 2003 - 
TL;DR: It is shown that ARF interacts with B23, a multifunctional nucleolar protein involved in ribosome biogenesis, and promotes its polyubiquitination and degradation, and suggests a nucleolar role of ARF in surveillance of oncogenic insults.
Journal ArticleDOI

Control of the Replicative Life Span of Human Fibroblasts by p16 and the Polycomb Protein Bmi-1

Koji Itahana, +10 more
- 01 Jan 2003 - 
TL;DR: It is reported that Bmi-1 is downregulated when WI-38 human fibroblasts undergo replicative senescence, but not quiescence, and extends replicative life span when overexpressed, and suggested that some human Fibroblast strains are more sensitive to stress-inducedsenescence and have both p16-dependent and p53/telomere-dependent pathways of senescENCE.
Journal ArticleDOI

Regulation of a Senescence Checkpoint Response by the E2F1 Transcription Factor and p14 ARF Tumor Suppressor

Goberdhan P. Dimri, +3 more
- 01 Jan 2000 - 
TL;DR: It is shown that E2F1, a multifunctional transcription factor that binds the retinoblastoma (pRb) tumor suppressor and that can either promote or suppress tumorigenesis, induces a senescent phenotype when overexpressed in normal human fibroblasts and identifies p14ARF as a potentially important mediator of the senescence phenotype.
Book ChapterDOI

Methods to detect biomarkers of cellular senescence: the senescence-associated beta-galactosidase assay.

Koji Itahana, +2 more
- 01 Jan 2007 - 
TL;DR: In this article, the authors described a biomarker associated with the senescent phenotype, a senescence associated beta-galactosidase (SA-beta-gal), which is detected by histochemical staining of cells using the artificial substrate X-gal.