K
Kishor K. Bhakat
Researcher at University of Nebraska Medical Center
Publications - 24
Citations - 1050
Kishor K. Bhakat is an academic researcher from University of Nebraska Medical Center. The author has contributed to research in topics: DNA repair & Base excision repair. The author has an hindex of 13, co-authored 24 publications receiving 911 citations.
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Journal ArticleDOI
Kruppel-like factor 4 is acetylated by p300 and regulates gene transcription via modulation of histone acetylation.
TL;DR: The results suggest that KLF4 might function as an activator or repressor of transcription depending on whether it interacts with co-activators such as p300 and CREB-binding protein or co-repressors such as HDAC3.
Journal ArticleDOI
Preferential repair of oxidized base damage in the transcribed genes of mammalian cells.
Dibyendu Banerjee,Santi M. Mandal,Aditi Das,Muralidhar L. Hegde,Soumita Das,Kishor K. Bhakat,Istvan Boldogh,Partha S. Sarkar,Sankar Mitra,Tapas K. Hazra +9 more
TL;DR: It is shown that the oxidized base-specific human DNA glycosylase NEIL2 associates with RNA polymerase II and the transcriptional regulator heterogeneous nuclear ribonucleoprotein-U (hnRNP-U), both in vitro and in cells.
Journal Article
Multifaceted Resistance of Gliomas to Temozolomide
Dora Bocangel,Sydney D. Finkelstein,S. Clifford Schold,Kishor K. Bhakat,Sankar Mitra,Demetrius M. Kokkinakis +5 more
TL;DR: By testing a limited number of glial tumors in cell culture and also as xenografts, it is shown that mobilization of the p53 in response to TMZ damage is likely to induce a cell cycle arrest and apoptosis inglial tumors.
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Intracellular trafficking and regulation of mammalian AP-endonuclease 1 (APE1), an essential DNA repair protein.
Sankar Mitra,Tadahide Izumi,Istvan Boldogh,Kishor K. Bhakat,Ranajoy Chattopadhyay,Bartosz Szczesny +5 more
TL;DR: It is shown that apoptosis of mouse embryo fibroblasts triggered by APE1 inactivation can be prevented by ectopic expression of repair competent but not repair-defective APE 1, consistent with the hypothesis that aging is associated with chronic oxidative stress.
Journal Article
p53-Mediated down-regulation of the human DNA repair gene O6-methylguanine-DNA methyltransferase (MGMT) via interaction with Sp1 transcription factor.
TL;DR: It is reported that p53 sequesters the Sp1 transcription factor to prevent its binding to the cognate cis elements in the MGMT promoter and thus inhibits MGMT expression, thus enhancing sensitivity of tumor cells to O(6)-alkylguanine generating drugs.