Distinct functions of wild-type and R273H mutant Δ133p53α differentially regulate glioblastoma aggressiveness and therapy-induced senescence.

Autor: Joruiz SM; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institute of Health, Bethesda, MD, USA., Von Muhlinen N; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institute of Health, Bethesda, MD, USA., Horikawa I; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institute of Health, Bethesda, MD, USA., Gilbert MR; Neuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA., Harris CC; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institute of Health, Bethesda, MD, USA. harrisc@mail.nih.gov.

Publikováno v: Cell death & disease [Cell Death Dis] 2024 Jun 27; Vol. 15 (6), pp. 454. Date of Electronic Publication: 2024 Jun 27.

Enhancing chimeric antigen receptor T cell therapy by modulating the p53 signaling network with Δ133p53α.

Autor: Roselle C; Center for Cellular Immunotherapies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.; Pharmacology Graduate Group, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., Horikawa I; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892., Chen L; Center for Cellular Immunotherapies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., Kelly AR; Center for Cellular Immunotherapies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., Gonzales D; Center for Cellular Immunotherapies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., Da T; Center for Cellular Immunotherapies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., Wellhausen N; Center for Cellular Immunotherapies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.; Pharmacology Graduate Group, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., Rommel PC; Center for Cellular Immunotherapies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.; Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., Baker D; Center for Cellular Immunotherapies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.; Pharmacology Graduate Group, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.; Cardiovascular Institute, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., Suhoski M; Center for Cellular Immunotherapies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., Scholler J; Center for Cellular Immunotherapies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., O'Connor RS; Center for Cellular Immunotherapies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., Young RM; Center for Cellular Immunotherapies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.; Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., Harris CC; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892., June CH; Center for Cellular Immunotherapies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.; Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.

Publikováno v: Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2024 Mar 05; Vol. 121 (10), pp. e2317735121. Date of Electronic Publication: 2024 Feb 26.

Downregulation of splicing factor SRSF3 induces p53β, an alternatively spliced isoform of p53 that promotes cellular senescence.

Autor: Tang, Y¹, Horikawa, I¹, Ajiro, M², Robles, A I¹, Fujita, K¹, Mondal, A M¹, Stauffer, J K³, Zheng, Z-M², Harris, C C¹

Publikováno v: Oncogene. 5/30/2013, Vol. 32 Issue 22, p2792-2798. 7p. 4 Diagrams.

Chronic social defeat stress increases the amounts of 12-lipoxygenase lipid metabolites in the nucleus accumbens of stress-resilient mice.

Autor: Akiyama S; Division of Pharmacology, Graduate School of Medicine, Kobe University, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.; Department of CNS Research, Otsuka Pharmaceutical Co., Ltd., Tokushima, 771-0192, Japan., Nagai H; Division of Pharmacology, Graduate School of Medicine, Kobe University, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.; Japan Agency for Medical Research and Development, Tokyo, 100-0004, Japan., Oike S; Division of Pharmacology, Graduate School of Medicine, Kobe University, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.; Japan Agency for Medical Research and Development, Tokyo, 100-0004, Japan., Horikawa I; Division of Pharmacology, Graduate School of Medicine, Kobe University, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.; Japan Agency for Medical Research and Development, Tokyo, 100-0004, Japan., Shinohara M; Japan Agency for Medical Research and Development, Tokyo, 100-0004, Japan.; Department of Community Medicine and Social Healthcare Science, Division of Epidemiology, Graduate School of Medicine, Kobe University, Kobe, 650-0017, Japan.; The Integrated Center for Mass Spectrometry, Graduate School of Medicine, Kobe University, Kobe, 650-0017, Japan., Lu Y; Division of Pharmacology, Graduate School of Medicine, Kobe University, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.; Japan Agency for Medical Research and Development, Tokyo, 100-0004, Japan., Futamura T; Department of CNS Research, Otsuka Pharmaceutical Co., Ltd., Tokushima, 771-0192, Japan., Shinohara R; Division of Pharmacology, Graduate School of Medicine, Kobe University, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.; Japan Agency for Medical Research and Development, Tokyo, 100-0004, Japan., Kitaoka S; Division of Pharmacology, Graduate School of Medicine, Kobe University, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.; Japan Agency for Medical Research and Development, Tokyo, 100-0004, Japan.; Department of Pharmacology, School of Medicine, Hyogo Medical University, Nishinomiya, 663-8501, Japan., Furuyashiki T; Division of Pharmacology, Graduate School of Medicine, Kobe University, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan. tfuruya@med.kobe-u.ac.jp.; Japan Agency for Medical Research and Development, Tokyo, 100-0004, Japan. tfuruya@med.kobe-u.ac.jp.

Publikováno v: Scientific reports [Sci Rep] 2022 Jul 05; Vol. 12 (1), pp. 11385. Date of Electronic Publication: 2022 Jul 05.

CircSMAD3 represses VSMC phenotype switching and neointima formation via promoting hnRNPA1 ubiquitination degradation.

Autor: Mei, Shuai^1,2 (AUTHOR), Ma, Xiaozhu^1,2 (AUTHOR), Zhou, Li^1,2 (AUTHOR), Wuyun, Qidamugai^1,2 (AUTHOR), Cai, Ziyang^1,2 (AUTHOR), Yan, Jiangtao^1,2 (AUTHOR) jtyan@tjh.tjmu.edu.cn, Ding, Hu^1,2 (AUTHOR) huding@tjh.tjmu.edu.cn

Publikováno v: Cell Proliferation. Jan2025, Vol. 58 Issue 1, p1-17. 17p.