Co-Authors
This is a "connection" page, showing publications co-authored by Carl Maki and Ricardo Perez.
Connection Strength
4.131
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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.
Score: 0.713
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Modeling the Etiology of p53-mutated Cancer Cells. J Biol Chem. 2016 May 06; 291(19):10131-47.
Score: 0.521
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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.
Score: 0.208
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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.
Score: 0.208
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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.
Score: 0.197
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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).
Score: 0.195
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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.
Score: 0.195
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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.
Score: 0.195
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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.
Score: 0.190
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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.
Score: 0.161
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JMJD2 promotes acquired cisplatin resistance in non-small cell lung carcinoma cells. Oncogene. 2019 07; 38(28):5643-5657.
Score: 0.161
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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.
Score: 0.155
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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.
Score: 0.153
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DZNep represses Bcl-2 expression and modulates apoptosis sensitivity in response to Nutlin-3a. Cancer Biol Ther. 2018 06 03; 19(6):465-474.
Score: 0.149
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The IGF-1R/AKT pathway has opposing effects on Nutlin-3a-induced apoptosis. Cancer Biol Ther. 2017 Nov 02; 18(11):895-903.
Score: 0.142
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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.
Score: 0.131
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p53-regulated autophagy is controlled by glycolysis and determines cell fate. Oncotarget. 2015 Sep 15; 6(27):23135-56.
Score: 0.125
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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.
Score: 0.115
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Increasing cisplatin sensitivity by schedule-dependent inhibition of AKT and Chk1. Cancer Biol Ther. 2014; 15(12):1600-12.
Score: 0.111
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Two 4N cell-cycle arrests contribute to cisplatin-resistance. PLoS One. 2013; 8(4):e59848.
Score: 0.106