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Connection

Lei Duan to Humans

This is a "connection" page, showing publications Lei Duan has written about Humans.
Connection Strength

0.645
  1. Novel markers of MCL1 inhibitor sensitivity in triple-negative breast cancer cells. J Biol Chem. 2024 Jun; 300(6):107375.
    View in: PubMed
    Score: 0.053
  2. CSE1L is a negative regulator of the RB-DREAM pathway in p53 wild-type NSCLC and can be targeted using an HDAC1/2 inhibitor. Sci Rep. 2023 09 27; 13(1):16271.
    View in: PubMed
    Score: 0.050
  3. 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.
    View in: PubMed
    Score: 0.048
  4. 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.
    View in: PubMed
    Score: 0.045
  5. 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.
    View in: PubMed
    Score: 0.044
  6. 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.
    View in: PubMed
    Score: 0.037
  7. JMJD2 promotes acquired cisplatin resistance in non-small cell lung carcinoma cells. Oncogene. 2019 07; 38(28):5643-5657.
    View in: PubMed
    Score: 0.037
  8. 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.
    View in: PubMed
    Score: 0.036
  9. 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.
    View in: PubMed
    Score: 0.035
  10. p53-regulated autophagy is controlled by glycolysis and determines cell fate. Oncotarget. 2015 Sep 15; 6(27):23135-56.
    View in: PubMed
    Score: 0.029
  11. Critical roles for nitric oxide and ERK in the completion of prosurvival autophagy in 4OHTAM-treated estrogen receptor-positive breast cancer cells. Cancer Lett. 2014 Oct 28; 353(2):290-300.
    View in: PubMed
    Score: 0.027
  12. 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.
    View in: PubMed
    Score: 0.026
  13. Increasing cisplatin sensitivity by schedule-dependent inhibition of AKT and Chk1. Cancer Biol Ther. 2014; 15(12):1600-12.
    View in: PubMed
    Score: 0.026
  14. Prolylcarboxypeptidase regulates proliferation, autophagy, and resistance to 4-hydroxytamoxifen-induced cytotoxicity in estrogen receptor-positive breast cancer cells. J Biol Chem. 2011 Jan 28; 286(4):2864-76.
    View in: PubMed
    Score: 0.021
  15. Negative regulation of EGFR-Vav2 signaling axis by Cbl ubiquitin ligase controls EGF receptor-mediated epithelial cell adherens junction dynamics and cell migration. J Biol Chem. 2011 Jan 07; 286(1):620-33.
    View in: PubMed
    Score: 0.021
  16. Distinct roles for Rho versus Rac/Cdc42 GTPases downstream of Vav2 in regulating mammary epithelial acinar architecture. J Biol Chem. 2010 Jan 08; 285(2):1555-68.
    View in: PubMed
    Score: 0.019
  17. Cbl-mediated ubiquitinylation is required for lysosomal sorting of epidermal growth factor receptor but is dispensable for endocytosis. J Biol Chem. 2003 Aug 01; 278(31):28950-60.
    View in: PubMed
    Score: 0.012
  18. Mixed lineage kinase 3 and CD70 cooperation sensitize trastuzumab-resistant HER2+ breast cancer by ceramide-loaded nanoparticles. Proc Natl Acad Sci U S A. 2022 09 20; 119(38):e2205454119.
    View in: PubMed
    Score: 0.012
  19. 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.
    View in: PubMed
    Score: 0.010
  20. DZNep represses Bcl-2 expression and modulates apoptosis sensitivity in response to Nutlin-3a. Cancer Biol Ther. 2018 06 03; 19(6):465-474.
    View in: PubMed
    Score: 0.009
  21. The IGF-1R/AKT pathway has opposing effects on Nutlin-3a-induced apoptosis. Cancer Biol Ther. 2017 Nov 02; 18(11):895-903.
    View in: PubMed
    Score: 0.008
  22. 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.
    View in: PubMed
    Score: 0.008
  23. Modeling the Etiology of p53-mutated Cancer Cells. J Biol Chem. 2016 May 06; 291(19):10131-47.
    View in: PubMed
    Score: 0.007
  24. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition). Autophagy. 2016; 12(1):1-222.
    View in: PubMed
    Score: 0.007
  25. Overexpression of RhoA induces preneoplastic transformation of primary mammary epithelial cells. Cancer Res. 2009 Jan 15; 69(2):483-91.
    View in: PubMed
    Score: 0.005
  26. Binding of Cbl to a phospholipase Cgamma1-docking site on platelet-derived growth factor receptor beta provides a dual mechanism of negative regulation. J Biol Chem. 2007 Oct 05; 282(40):29336-47.
    View in: PubMed
    Score: 0.004
  27. A critical role for the E3-ligase activity of c-Cbl in VEGFR-2-mediated PLCgamma1 activation and angiogenesis. Proc Natl Acad Sci U S A. 2007 Mar 27; 104(13):5413-8.
    View in: PubMed
    Score: 0.004
  28. Biochemical basis for the requirement of kinase activity for Cbl-dependent ubiquitinylation and degradation of a target tyrosine kinase. J Biol Chem. 2004 Aug 20; 279(34):36132-41.
    View in: PubMed
    Score: 0.003
  29. Cbl-mediated ubiquitinylation and negative regulation of Vav. J Biol Chem. 2003 Oct 03; 278(40):38495-504.
    View in: PubMed
    Score: 0.003
Connection Strength

The connection strength for concepts is the sum of the scores for each matching publication.

Publication scores are based on many factors, including how long ago they were written and whether the person is a first or senior author.