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Cell genomics 2025年 100888页

作者： Fengshuo Liu Yunfeng Ding Zhan Xu Xiaoxin Hao Tianhong Pan George Miles Siyue Wang Yi-Hsuan Wu Jun Liu Igor L Bado Weijie Zhang Ling Wu Yang Gao Liqun Yu David G Edwards Hilda L Chan Sergio Aguirre Michael Warren Dieffenbach Elina Chen Yichao Shen Dane Hoffman Luis Becerra Dominguez Charlotte Helena Rivas Xiang Chen Hai Wang Zbigniew Gugala Robert L Satcher Xiang H-F Zhang Lester and Sue Smith Breast Center Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA Dan L. Duncan Cancer Center Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA Department of Molecular and Cellular Biology Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA Graduate Program in Cancer and Cell Biology Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA. Department of Molecular and Cellular Biology Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA. Department of Orthopedic Oncology University of Texas MD Anderson Cancer Center Houston TX USA. Dan L. Duncan Cancer Center Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA. Graduate Program in Immunology and Microbiology Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA. Medical Scientist Training Program Baylor College of Medicine Houston TX 77030 USA. Graduate Program in Cancer and Cell Biology Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA Graduate Program in Integrative Molecular and Biomedical Sciences Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA. Graduate Program in Development Disease Models and Therapeutics Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA. College of Natural Sciences University of Texas at Austin 110 Inner Campus Drive Austin TX 78706 USA. Department of Orthopedic Surgery and Rehabilitation University of Texas Medical Branch Galveston TX USA. Department of Orthopedic Oncology University of Texas MD Anderson Cancer Center Houston TX USA. Electronic address: rlsatcher@***. McNair Medical Institute Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA. Electronic address: xiangz@bcm.edu.

Bone is a common site for metastasis of solid cancers. The diversity of histological and molecular characteristics of bone metastases (BMs) remains poorly studied. Here, we performed single-cell RNA sequencing on 42 BMs from eight cancer types, identifying three distinct ecosystem archetypes, each characterized by an enrichment of specific immune cells: macrophages/osteoclasts, regulatory/exhausted T cells, or monocytes. We validated these archetypes by immunostaining on tissue sections and bioinformatic analysis of bulk RNA sequencing/microarray data from 158 BMs across more than 10 cancer types. Interestingly, we found only a modest correlation between the BM archetypes and the tissues of origin; BMs from the same cancer type often fell into different archetypes, while BMs from different cancer types sometimes converged on the same archetype. Additional analyses revealed parallel immunosuppression and bone remodeling mechanisms, some of which were experimentally validated. Overall, we discovered unappreciated heterogeneity of BMs across different cancers.

关键词： bone metastases convergent and divergent evolution immune archetypes immune evasion immunosuppression single-cell RNA sequencing tumor microenvironment

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A Kinetic Scout Approach Accelerates Targeted Protein Degrader Development

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Angewandte Chemie 2024年第5期137卷

作者： Angela T. Fan Gillian E. Gadbois Hai-Tsang Huang Charu Chaudhry Jiewei Jiang Logan H. Sigua Emily R. Smith Sitong Wu Grace J. Poirier Kara Dunne-Dombrink Pavitra Goyal Andrew J. Tao William R. Sellers Eric S. Fischer Katherine A. Donovan Fleur M. Ferguson Department of Chemistry and Biochemistry University of California San Diego The Broad Institute of Harvard and MIT Department of Medical Oncology Dana-Farber Cancer Institute Harvard Medical School Boston Discovery Technologies Molecular Pharmacology J&J Innovative Medicine Spring House Pennsylvania 19477 United States Medical Scientist Training Program University of California San Diego Department of Cancer Biology Dana-Farber Cancer Institute Boston Department of Biological Chemistry and Molecular Pharmacology Harvard Medical School Boston Skaggs School of Pharmacy and Pharmaceutical Sciences University of California San Diego

Bifunctional molecules such as targeted protein degraders induce proximity to promote gain-of-function pharmacology. These powerful approaches have gained broad traction across academia and the pharmaceutical industry, leading to an intensive focus on strategies that can accelerate their identification and optimization. We and others have previously used chemical proteomics to map degradable target space, and these datasets have been used to develop and train multiparameter models to extend degradability predictions across the proteome. In this study, we now turn our attention to develop generalizable chemistry strategies to accelerate the development of new bifunctional degraders. We implement lysine-targeted reversible-covalent chemistry to rationally tune the binding kinetics at the protein-of-interest across a set of 25 targets. We define an unbiased workflow consisting of global proteomics analysis, IP/MS of ternary complexes and the E-STUB assay, to mechanistically characterize the effects of ligand residence time on targeted protein degradation and formulate hypotheses about the rate-limiting step of degradation for each target. Our key finding is that target residence time is a major determinant of degrader activity, and this can be rapidly and rationally tuned through the synthesis of a minimal number of analogues to accelerate early degrader discovery and optimization.

关键词： Targeted protein degradation PROTACs compound residence time proteomics proteasomal degradation

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Proliferative and metastatic roles for Phospholipase D in mouse models of cancer

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Advances in Biological Regulation 2018年 67卷 134-140页

作者： Roth, Eric Frohman, Michael A. The Graduate Program in Molecular and Cellular Pharmacology The Medical Scientist Training Program the Department of Pharmacological Sciences Stony Brook University New York 11794 United States

Phospholipase D (PLD) activity has been proposed to facilitate multiple steps in cancer progression including growth, metabolism, angiogenesis, and mobility. The canonical enzymes PLD1 and PLD2 enact their diverse effects through hydrolyzing the membrane lipid phosphatidylcholine to generate the second messenger and signaling lipid phosphatidic acid (PA). However, the widespread expression of PLD1 and PLD2 in normal tissues and the additional distinct enzymatic mechanisms through which PA can be generated have produced uncertainty regarding the optimal settings in which PLD inhibition might ameliorate cancer. Recent studies in mouse model systems have demonstrated that inhibition or elimination of PLD activity reduces tumor growth and metastasis. One mechanism proposed for this outcome involves proliferative signaling mediated by receptor tyrosine kinases (RTK) and G protein-coupled receptors (GPCR), which is attenuated when downstream PLD signal propagation is suppressed. The reduced proliferative signaling has been reported to be compounded by dysfunctional energetic metabolism in the tumor cells under conditions of nutrient deprivation. Moreover, cancer cells lacking PLD activity display inefficiencies across multiple steps of the metastatic cascade, limiting the tumor's lethal spread. Using PLD isoform knockout mice, recent studies have reported on the net effects of inhibition and ablation in multiple cancer models through examining the role of PLD in the non-tumor cells comprising the stroma and microenvironment. The promising results of such in vivo studies, combined with the apparent low toxicity of highly-specific and potent inhibitors, highlights PLD as an attractive target for therapeutic inhibition in cancer. We discuss here the array of anti-tumor effects produced by PLD inhibition and ablation in cancer models with a focus on animal studies. © 2017 Elsevier Ltd

关键词： Angiogenesis Cancer Lipid signaling Metabolism Metastasis Phospholipase D

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Correction to: USP20 positively regulates tumorigenesis and chemoresistance through β-catenin stabilization

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Cell death and differentiation 2023年第3期30卷 857-858页

作者： Chenming Wu Kuntian Luo Fei Zhao Ping Yin Ying Song Min Deng Jinzhou Huang Yuping Chen Lei Li SeungBaek Lee JungJin Kim Qin Zhou Xinyi Tu Somaira Nowsheen Qifeng Luo Xiumei Gao Zhenkun Lou Zhongmin Liu Jian Yuan Research Center for Translational Medicine East Hospital Tongji University School of Medicine Shanghai 200120 China. Key Laboratory of Arrhythmias of the Ministry of Education of China East Hospital Tongji University School of Medicine Shanghai 200120 China. Department of Oncology Mayo Clinic Rochester MN 55905 USA. Department of Pathology East Hospital Shanghai 200120 China. Mayo Clinic Medical Scientist Training Program Mayo Clinic School of Medicine and Mayo Clinic Graduate School of Biomedical Sciences Mayo Clinic Rochester MN 55905 USA. Department of Molecular Pharmacology and Experimental Therapeutics Mayo Clinic Rochester MN 55905 USA. Department of Gastrointestinal Surgery Shanghai East Hospital School of Medicine Tongji University Shanghai 200120 Shanghai P. R. China. Tianjin State Key Laboratory of Modern Chinese Medicine Tianjin University of Traditional Chinese Medicine 300193 Tianjin China. Department of Oncology Mayo Clinic Rochester MN 55905 USA. Lou.zhenkun@mayo.edu. Research Center for Translational Medicine East Hospital Tongji University School of Medicine Shanghai 200120 China. Zhongmin_Liu@***. Key Laboratory of Arrhythmias of the Ministry of Education of China East Hospital Tongji University School of Medicine Shanghai 200120 China. Zhongmin_Liu@***. Research Center for Translational Medicine East Hospital Tongji University School of Medicine Shanghai 200120 China. Yuanjian229@***. Key Laboratory of Arrhythmias of the Ministry of Education of China East Hospital Tongji University School of Medicine Shanghai 200120 China. Yuanjian229@***. Department of Oncology Mayo Clinic Rochester MN 55905 USA. Yuanjian229@***. Department of Molecular Pharmacology and Experimental Therapeutics Mayo Clinic Rochester MN 55905 USA. Yuanjian229@***.

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CD38-CAR human NK cells in combination with ATRA enhance cytotoxicity against CD38-expressing hematologic malignancies

Blood Neoplasia

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Blood Neoplasia 2024年第4期1卷 100032-100032页

作者： Ella Troy Joseph Caporale Yasemin Sezgin Marcelo S. F. Pereira Gregory Behbehani Justin Lyberger Dean A. Lee Meisam Naeimi Kararoudi Center for Childhood Cancer Abigail Wexner Research Institute at Nationwide Children’s Hospital Columbus OH Medical Scientist Training Progam The Ohio State University College of Medicine Columbus OH Molecular Cellular Developmental Biology Program The Ohio State University Columbus OH Department of Medicine Division of Hematology The Ohio State University Comprehensive Cancer Center The Ohio State University Columbus OH Department of Pediatrics The Ohio State University Columbus OH

Abstract CD38 is a metabolically active enzyme broadly expressed on the surface of normal and malignant hematologic cells. It has been targeted clinically with anti-CD38 monoclonal antibodies (mAbs), for which efficacy may be limited by natural killer (NK)–cell fratricide. Isatuximab is an anti-CD38 mAb that uniquely inhibits CD38 metabolic activity. Here, we used CRISPR/adeno-associated virus (AAV) to generate fratricide–resistant and metabolically–enhanced CD38 KO /CD38-chimeric antigen receptor (CAR) NK cells using 2 isatuximab-based CD38 single-chain variable fragments (scFvs; reversing heavy and light chain orientation) on the same CD8α/4-1BB/CD3ζ base, and we demonstrate their activity against a range of CD38 + hematologic malignancies (acute myeloid leukemia, multiple myeloma, Burkitt lymphoma, and T-cell leukemia/lymphoma). The cytotoxicity of the CAR NK cells was enhanced by upregulating CD38 expression on the malignant targets with all-trans retinoic acid (ATRA). By generating CD38 KO /CD38-CAR T cells using the same engineering approach, we show that the CAR NK cells had higher cytotoxicity than CAR T cells against all hematologic tumor targets. Additionally, AAVS1 KO /CD38-CAR NK cells were capable of targeting CD38 without experiencing fratricide and have a similar enhanced metabolic activity via the inhibitory activity of the cis-acting isatuximab-based scFv. Finally, we report fratricide-resistant CD38-CAR NK cells with enhanced metabolism and cytotoxicity toward CD38 + hematologic malignancies, further increased by combination treatment with ATRA.

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Correction to: Droplet Hi-C enables scalable, single-cell profiling of chromatin architecture in heterogeneous tissues (Nature Biotechnology, (2024), 10.1038/s41587-024-02447-1)

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Nature Biotechnology 2025年

作者： Chang, Lei Xie, Yang Taylor, Brett Wang, Zhaoning Sun, Jiachen Armand, Ethan J. Mishra, Shreya Xu, Jie Tastemel, Melodi Lie, Audrey Gibbs, Zane A. Indralingam, Hannah S. Tan, Tuyet M. Bejar, Rafael Chen, Clark C. Furnari, Frank B. Hu, Ming Ren, Bing Department of Cellular and Molecular Medicine University of California San Diego La JollaCA United States Biomedical Sciences Graduate Program University of California San Diego La JollaCA United States Medical Scientist Training Program University of California San Diego La JollaCA United States Department of Quantitative Health Sciences Lerner Research Institute Cleveland Clinic Foundation ClevelandOH United States Systems Biology and Bioinformatics PhD Program Case Western Reserve University School of Medicine ClevelandOH United States Bioinformatics and Systems Biology Program University of California San Diego La JollaCA United States Moores Cancer Center UC San Diego La JollaCA United States Department of Neurosurgery University of Minnesota MinneapolisMN United States Department of Medicine University of California San Diego School of Medicine La JollaCA United States Center for Epigenomics Institute for Genomic Medicine School of Medicine University of California San Diego La JollaCA United States

Correction to: Nature Biotechnologyhttps://***/10.1038/s41587-024-02447-1, published online 18 October 2024. In the version of the article initially published, in the Methods section, both mentions of "MboII" should have read "MboI (NEB, R0147M)" and have now been corrected in the HTML and PDF versions of the article. © The Author(s) 2025.

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Correction: SNCA genetic lowering reveals differential cognitive function of alpha-synuclein dependent on sex

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Acta neuropathologica communications 2024年第1期12卷 92页

作者： Jennifer L Brown Damyan W Hart Gabriel E Boyle Taylor G Brown Michael LaCroix Andrés M Baraibar Ross Pelzel Minwoo Kim Mathew A Sherman Samuel Boes Michelle Sung Tracy Cole Michael K Lee Alfonso Araque Sylvain E Lesné Graduate Program in Neuroscience University of Minnesota Minneapolis MN USA. Department of Neuroscience University of Minnesota Minneapolis MN USA. Institute for Translational Neuroscience University of Minnesota Wallin Medical Biosciences Building (Room 4-114) 2101 Sixth Street SE CDC 2641 Minneapolis MN 55414 USA. Graduate Program in Molecular and Cellular Biology University of Washington Seattle WA 98195 USA. Medical Scientist Training Program University of Minnesota Minneapolis MN USA. Medical Scientist Training Program University of Texas Southwestern Medical School Dallas TX 75390 USA. Department of Neurosciences University of the Basque Country UPV/EHU Leioa Spain. Bloomberg School of Public Health Johns Hopkins University Baltimore MD 21218 USA. Ionis Pharmaceuticals Inc. Carlsbad CA USA. n-Lorem Foundation Carlsbad CA 92010 USA. Graduate Program in Neuroscience University of Minnesota Minneapolis MN USA. lesne002@umn.edu. Department of Neuroscience University of Minnesota Minneapolis MN USA. lesne002@umn.edu. Institute for Translational Neuroscience University of Minnesota Wallin Medical Biosciences Building (Room 4-114) 2101 Sixth Street SE CDC 2641 Minneapolis MN 55414 USA. lesne002@umn.edu.

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Defining new mechanistic roles for α II spectrin in cardiac function (vol 294, pg 9576, 2019)

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JOURNAL OF BIOLOGICAL CHEMISTRY 2019年第42期294卷 15557-15557页

作者： Lubbers, Ellen R. Murphy, Nathaniel P. Musa, Hassan Huang, Claire Yu-Mei Gupta, Rohan Price, Morgan V. Han, Mei Daoud, Georges E. Gratz, Daniel El Refaey, Mona Xu, Xianyao Hoeflinger, Nicole K. Friel, Emma L. Lancione, Peter Wallace, Michael J. Cavus, Omer Simmons, Samantha L. Williams, Jordan L. Skaf, Michel Koenig, Sara N. Janssen, Paul M. L. Rasband, Matthew N. Hund, Thomas J. Mohler, Peter J. From the [‡]Dorothy M. Davis Heart and Lung Research Institute and Frick Center for Heart Failure and Arrhythmia [§]Medical Scientist Training Program the Departments of [¶]Physiology and Cell Biology and [‡‡]Internal Medicine Division of Cardiovascular Medicine The Ohio State University College of Medicine and Wexner Medical Center Columbus Ohio 432310 the [‖]Department of Neuroscience and Integrative Molecular and Biomedical Sciences Graduate Program Baylor College of Medicine Houston Texas 77030 and the [**]Department of Biomedical Engineering The Ohio State University Columbus Ohio 432310 ↵To whom correspondence should be addressed: 110G DHLRI 473 West 12th Ave. Columbus OH 43210. Tel.: 614-292-5019 Fax: 614-247-7799 E-mail: Peter.Mohler{at}osumc.edu.

Spectrins are cytoskeletal proteins essential for membrane biogenesis and regulation and serve critical roles in protein targeting and cellular signaling. αII spectrin (SPTAN1) is one of two α spectrin genes and αII spectrin dysfunction is linked to alterations in axon initial segment formation, cortical lamination, and neuronal excitability. Furthermore, human αII spectrin loss-of-function variants cause neurological disease. As global αII spectrin knockout mice are embryonic lethal, the in vivo roles of αII spectrin in adult heart are unknown and untested. Here, based on pronounced alterations in αII spectrin regulation in human heart failure we tested the in vivo roles of αII spectrin in the vertebrate heart. We created a mouse model of cardiomyocyte-selective αII spectrin-deficiency (cKO) and used this model to define the roles of αII spectrin in cardiac function. αII spectrin cKO mice displayed significant structural, cellular, and electrical phenotypes that resulted in accelerated structural remodeling, fibrosis, arrhythmia, and mortality in response to stress. At the molecular level, we demonstrate that αII spectrin plays a nodal role for global cardiac spectrin regulation, as αII spectrin cKO hearts exhibited remodeling of αI spectrin and altered β-spectrin expression and localization. At the cellular level, αII spectrin deficiency resulted in altered expression, targeting, and regulation of cardiac ion channels Na_V1.5 and K_V4.3. In summary, our findings define critical and unexpected roles for the multifunctional αII spectrin protein in the heart. Furthermore, our work provides a new in vivo animal model to study the roles of αII spectrin in the cardiomyocyte.

关键词： heart heart failure adaptor protein ion channel cardiovascular disease cytoskeleton spectrin ankryin

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Angiotensin AT 1 R expressing cells within the ventral hypothalamus modulate integrative control of cardiometabolic functions

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iScience 2025年第7期28卷

作者： Jhonatan Pasos Valerie A. Wagner Samuel B.R. Lawton Alyssa M. Madison Kush Nandani Natalia M. Mathieu Connie C. Grobe John J. Reho Bonnie P. Freudinger Alexander J. Sherman Daniel T. Brozoski Lisa L. Morselli Colin M.L. Burnett Jeffrey L. Segar Pablo Nakagawa Curt D. Sigmund Justin L. Grobe Department of Physiology Medical College of Wisconsin Milwaukee WI 53226 USA Universidad CES Medellin Antioquia Colombia Medical Scientist Training Program Medical College of Wisconsin Milwaukee WI 53226 USA Department of Pediatrics Division of Neonatology Medical College of Wisconsin Milwaukee WI 53226 USA Comprehensive Rodent Metabolic Phenotyping Core Medical College of Wisconsin Milwaukee WI 53226 USA Engineering Core Medical College of Wisconsin Milwaukee WI 53226 USA Department of Medicine / Division of Endocrinology and Molecular Medicine Medical College of Wisconsin Milwaukee WI 53226 USA Cardiovascular Center Medical College of Wisconsin Milwaukee WI 53226 USA Department of Medicine / Division of Cardiovascular Medicine Medical College of Wisconsin Milwaukee WI 53226 USA Department of Biomedical Engineering Medical College of Wisconsin Milwaukee WI 53226 USA Neuroscience Research Center Medical College of Wisconsin Milwaukee WI 53226 USA

Subtypes of agouti-related peptide (AgRP) neurons can be distinguished based upon expression of angiotensin II receptors. The type 1 subtype, which expresses the angiotensin type 1 receptor ( Agtr1a ), was examined for its role in the integrative control of cardiometabolic functions. Mice expressing Cre-recombinase via the Agtr1a locus received bilateral microinjection of an AAV vector encoding Cre-dependent expression of caspase-3 into the arcuate nucleus of mice housed at 22°C or 30°C. Ablation of Agtr1a + cells caused increased food intake, adiposity, resting metabolic rate and shifts in nutrient partitioning, elevated temperature preference, loss of core temperature defense, and changes in blood pressure and heart rate. Many phenotypes were ameliorated by housing animals at thermoneutrality. Thus, Agtr1a + cells in the ventral hypothalamus (including the type 1 AgRP neuron) influence cardiometabolic control through modulation of thermoregulatory responses to cold. Some functions of these cells appear to oppose canonical roles of other AgRP neuron subtypes.

关键词： molecular biology Neuroscience Omics

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Microbiota-derived inosine programs protective CD8+ T cell responses against influenza in newborns

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Cell 2025年

作者： Stevens, Joseph Culberson, Erica Kinder, Jeremy Ramiriqui, Alicia Gray, Jerilyn Bonfield, Madeline Shao, Tzu-Yu Al Gharaibeh, Faris Peterson, Laura Steinmeyer, Shelby Eshleman, Emily M. Negi, Shikha Zacharias, William Pryhuber, Gloria Paul, Oindrila Sengupta, Shaon Alenghat, Theresa Way, Sing Sing Deshmukh, Hitesh Department of Pediatrics University of Cincinnati College of Medicine Cincinnati OH United States Division of Neonatology Cincinnati Children's Hospital Medical Center Cincinnati OH United States Medical Scientist Training Program University of Cincinnati College of Medicine Cincinnati OH United States Immunology Graduate Program Cincinnati Children's Hospital Medical Center Cincinnati OH United States Division of Infectious Disease Cincinnati Children's Hospital Medical Center Cincinnati OH United States Center for Inflammation and Tolerance Cincinnati Children's Hospital Medical Center Cincinnati OH United States Department of Pediatrics University of Louisville School of Medicine Louisville KY United States Division of Immunobiology Cincinnati Children's Hospital Medical Center Cincinnati OH United States Department of Pediatrics School of Medicine University of Rochester Rochester NY United States Division of Neonatology Children's Hospital of Philadelphia Perelman School of Medicine University of Pennsylvania Philadelphia PA United States

Early-life susceptibility to respiratory viral infections remains a major public health concern, yet the underlying mechanisms are poorly understood. We demonstrate that antibiotic-induced dysbiosis impairs influenza-specific CD8⁺ T cell immunity in infant mice and humans through the disruption of nuclear factor interleukin 3 (NFIL3)-dependent T cell programming. Mechanistically, we show that dysbiosis reduces intestinal and circulating inosine levels, disrupting NFIL3’s epigenetic regulation of T cell factor 1 (TCF1) expression. This leads to intrinsic defects in CD8⁺ T cell proliferation and differentiation, diminished effector responses, and impaired formation of tissue-resident memory cells. Bifidobacterium colonization restores intestinal and pulmonary inosine levels, establishing a specific pathway of gut-lung metabolic communication. Notably, inosine supplementation rescues NFIL3-dependent regulation of TCF1, enhancing CD8⁺ T cell responses and protection against influenza infection in dysbiotic infants. Our findings reveal how early-life microbial communities shape antiviral immunity and identify inosine as a therapeutic target for enhancing respiratory defenses in infants.

关键词： immunology infants influenza inosine microbiota T cell responses

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