Alpha ketoglutarate levels, regulated by p53 and OGDH, determine autophagy and cell fate/apoptosis in response to Nutlin-3a. Cancer Biol Ther. 2019; 20(3):252-260.
Alpha ketoglutarate levels, regulated by p53 and OGDH, determine autophagy and cell fate/apoptosis in response to Nutlin-3a.
Duan L, Perez RE, Chastain PD, Mathew MT, Bijukumar DR, Maki CG
JMJD2 promotes acquired cisplatin resistance in non-small cell lung carcinoma cells. Oncogene. 2019 07; 38(28):5643-5657.
JMJD2 promotes acquired cisplatin resistance in non-small cell lung carcinoma cells.
Duan L, Perez RE, Lai X, Chen L, Maki CG
The histone demethylase JMJD2B is critical for p53-mediated autophagy and survival in Nutlin-treated cancer cells. J Biol Chem. 2019 06 07; 294(23):9186-9197.
The histone demethylase JMJD2B is critical for p53-mediated autophagy and survival in Nutlin-treated cancer cells.
Faculty Profile at RUSH University Medical Center
Laboratory at RUSH University Medical Center
RUSH Cancer Center Biorepository Resource
Duan L, Ying G, Danzer B, Perez RE, Shariat-Madar Z, Levenson VV, Maki CG
The prolyl peptidases PRCP/PREP regulate IRS-1 stability critical for rapamycin-induced feedback activation of PI3K and AKT. J Biol Chem. 2014 Aug 01; 289(31):21694-705.
The prolyl peptidases PRCP/PREP regulate IRS-1 stability critical for rapamycin-induced feedback activation of PI3K and AKT.
Duan L, Perez RE, Hansen M, Gitelis S, Maki CG
Increasing cisplatin sensitivity by schedule-dependent inhibition of AKT and Chk1. Cancer Biol Ther. 2014; 15(12):1600-12.
Increasing cisplatin sensitivity by schedule-dependent inhibition of AKT and Chk1.
Duan L, Perez RE, Davaadelger B, Dedkova EN, Blatter LA, Maki CG
p53-regulated autophagy is controlled by glycolysis and determines cell fate. Oncotarget. 2015 Sep 15; 6(27):23135-56.
p53-regulated autophagy is controlled by glycolysis and determines cell fate.
Perez RE, Shen H, Duan L, Kim RH, Kim T, Park NH, Maki CG
Modeling the Etiology of p53-mutated Cancer Cells. J Biol Chem. 2016 May 06; 291(19):10131-47.
Modeling the Etiology of p53-mutated Cancer Cells.
Davaadelger B, Duan L, Perez RE, Gitelis S, Maki CG
Crosstalk between the IGF-1R/AKT/mTORC1 pathway and the tumor suppressors p53 and p27 determines cisplatin sensitivity and limits the effectiveness of an IGF-1R pathway inhibitor. Oncotarget. 2016 May 10; 7(19):27511-26.
Crosstalk between the IGF-1R/AKT/mTORC1 pathway and the tumor suppressors p53 and p27 determines cisplatin sensitivity and limits the effectiveness of an IGF-1R pathway inhibitor.
Shen H, Perez RE, Davaadelger B, Maki CG
Two 4N cell-cycle arrests contribute to cisplatin-resistance. PLoS One. 2013; 8(4):e59848.
Two 4N cell-cycle arrests contribute to cisplatin-resistance.
Perez RE, Calhoun S, Shim D, Levenson VV, Duan L, Maki CG
Prolyl endopeptidase inhibitor Y-29794 blocks the IRS1-AKT-mTORC1 pathway and inhibits survival and in vivo tumor growth of triple-negative breast cancer. Cancer Biol Ther. 2020 11 01; 21(11):1033-1040.
Prolyl endopeptidase inhibitor Y-29794 blocks the IRS1-AKT-mTORC1 pathway and inhibits survival and in vivo tumor growth of triple-negative breast cancer.
Duan L, Calhoun S, Shim D, Perez RE, Blatter LA, Maki CG
Fatty acid oxidation and autophagy promote endoxifen resistance and counter the effect of AKT inhibition in ER-positive breast cancer cells. J Mol Cell Biol. 2021 09 11; 13(6):433-444.
Fatty acid oxidation and autophagy promote endoxifen resistance and counter the effect of AKT inhibition in ER-positive breast cancer cells.
Corrigendum to 'Fatty acid oxidation and autophagy promote endoxifen resistance and counter the effect of AKT inhibition in ER-positive breast cancer cells'. J Mol Cell Biol. 2022 Jan 29; 13(12):922.
Corrigendum to 'Fatty acid oxidation and autophagy promote endoxifen resistance and counter the effect of AKT inhibition in ER-positive breast cancer cells'.
RBL2/DREAM-mediated repression of the Aurora kinase A/B pathway determines therapy responsiveness and outcome in p53 WT NSCLC. Sci Rep. 2022 01 20; 12(1):1049.
RBL2/DREAM-mediated repression of the Aurora kinase A/B pathway determines therapy responsiveness and outcome in p53 WT NSCLC.
Inhibitors of Jumonji C domain-containing histone lysine demethylases overcome cisplatin and paclitaxel resistance in non-small cell lung cancer through APC/Cdh1-dependent degradation of CtIP and PAF15. Cancer Biol Ther. 2022 12 31; 23(1):65-75.
Inhibitors of Jumonji C domain-containing histone lysine demethylases overcome cisplatin and paclitaxel resistance in non-small cell lung cancer through APC/Cdh1-dependent degradation of CtIP and PAF15.
Duan L, Calhoun S, Perez RE, Macias V, Mir F, Pergande MR, Gattuso P, Borgia JA, Maki CG
Prolyl Carboxypeptidase Maintains Receptor Tyrosine Kinase Signaling and Is a Potential Therapeutic Target in Triple Negative Breast Cancer. Cancers (Basel). 2022 Jan 31; 14(3).
Prolyl Carboxypeptidase Maintains Receptor Tyrosine Kinase Signaling and Is a Potential Therapeutic Target in Triple Negative Breast Cancer.
Author Correction: RBL2/DREAM-mediated repression of the Aurora kinase A/B pathway determines therapy responsiveness and outcome in p53 WT NSCLC. Sci Rep. 2022 Mar 16; 12(1):4525.
Author Correction: RBL2/DREAM-mediated repression of the Aurora kinase A/B pathway determines therapy responsiveness and outcome in p53 WT NSCLC.
Davaadelger B, Perez RE, Zhou Y, Duan L, Gitelis S, Maki CG
The IGF-1R/AKT pathway has opposing effects on Nutlin-3a-induced apoptosis. Cancer Biol Ther. 2017 Nov 02; 18(11):895-903.
The IGF-1R/AKT pathway has opposing effects on Nutlin-3a-induced apoptosis.
Duan L, Perez RE, Chen L, Blatter LA, Maki CG
p53 promotes AKT and SP1-dependent metabolism through the pentose phosphate pathway that inhibits apoptosis in response to Nutlin-3a. J Mol Cell Biol. 2018 08 01; 10(4):331-340.
p53 promotes AKT and SP1-dependent metabolism through the pentose phosphate pathway that inhibits apoptosis in response to Nutlin-3a.
Duan L, Calhoun SJ, Perez RE, Macias V, Mir F, Gattuso P, Maki CG
Prolylcarboxypeptidase promotes IGF1R/HER3 signaling and is a potential target to improve endocrine therapy response in estrogen receptor positive breast cancer. Cancer Biol Ther. 2022 Dec 31; 23(1):1-10.
Prolylcarboxypeptidase promotes IGF1R/HER3 signaling and is a potential target to improve endocrine therapy response in estrogen receptor positive breast cancer.
DZNep represses Bcl-2 expression and modulates apoptosis sensitivity in response to Nutlin-3a. Cancer Biol Ther. 2018 06 03; 19(6):465-474.
DZNep represses Bcl-2 expression and modulates apoptosis sensitivity in response to Nutlin-3a.