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BPS2025 - A general approach for improving the binding strength of cell-targeting aptamers

Biophysical Journal 2025年第3期124卷 106a-106a页

作者： Hari Priya Sriramakrishnan Qian Tian Lucy Luong Mingxu You Department of Chemistry University of Massachusetts Amherst Amherst MA USA Molecular and Cellular Biology Graduate Program University of Massachusetts Amherst Amherst MA USA

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ISOLATION AND CHARACTERIZATION OF 6 HEAT-SHOCK TRANSCRIPTION FACTOR CDNA CLONES FROM SOYBEAN

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PLANT molecular biology 1995年第1期29卷 37-51页

作者： CZARNECKAVERNER, E YUAN, CX FOX, PC GURLEY, WB Department of Microbiology and Cell Science Program of Plant Molecular and Cellular Biology University of Florida Gainesville USA

Thermal stress in soybean seedlings causes the activation of pre-existing heat shock transcription factor proteins (HSFs). Activation results in the induction of DNA binding activity which leads to the transcription of heat shock genes. From a soybean cDNA library we have isolated cDNA clones corresponding to six HSF genes. Two HSF genes are expressed constitutively at the transcriptional level, and the remaining four are heat-inducible. Two of the heat inducible genes are also responsive to cadmium stress. Comparative analysis of HSF sequences indicated higher conservation of the DNA binding domain among plant HSFs than those from yeast or other higher eukaryotes. The putative plant HSF oligomerization domain contains hydrophobic heptapeptide repeats characteristic of coiled coils and seems to exist in two structural variants. The carboxy-terminal domains are reduced in size and the C-terminal heptad repeat is degenerate.

关键词： HSF DNA BINDING DOMAIN OLIGOMERIZATION DOMAIN STRESS

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BPS2025 - Elucidating the nanoscale clustering profiles of chimeric antigen receptors

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Biophysical Journal 2025年第3期124卷 105a-105a页

作者： Robert J. Pyron Sarah Binion Sarah A. Shelby Genome Science and Technology Program University of Tennessee Knoxville TN USA Department of Biochemistry and Cellular and Molecular Biology University of Tennessee Knoxville TN USA

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BPS2025 - DNA barcode-based tools to visualize and modulate membrane protein-protein interactions

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Biophysical Journal 2025年第3期124卷 106a-106a页

作者： Yizhan Guo Ahsan Ausaf Ali Mingxu You Molecular and Cellular Biology Graduate Program University of Massachusetts Amherst Amherst MA USA Department of Chemistry University of Massachusetts Amherst Amherst MA USA

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PROTEIN-KINASE-C, A PIVOTAL REGULATOR OF HAMSTER EGG ACTIVATION, FUNCTIONS AFTER ELEVATION OF INTRAcellular FREE CALCIUM

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DEVELOPMENTAL biology 1993年第1期156卷 94-106页

作者： GALLICANO, GL SCHWARZ, SM MCGAUGHEY, RW CAPCO, DG Molecular and Cellular Biology Program Department of Zoology Arizona State University Tempe Arizona 85287-1501

We investigated the signal transduction pathways that mediate activation of Syrian hamster eggs. Under conditions in which the concentration of intracellular free calcium ([Ca 2+ ] i ) is clamped low, activation of protein kinase C (PKC) can induce second polar body formation, reformation of the nuclear envelope, and decondensation of chromatin, as well as golgi reformation. However, calcium is necessary for normal transition from meiotic metaphase II to anaphase II. Conversely, under conditions in which the level of PKC activity is clamped low, induction of a rise in [Ca 2+ ] i , using the calcium ionophore A23187, does not induce egg activation. These results strongly suggest that PKC acts after the calcium signal as a proximal inducer of egg activation. This suggestion is supported by the kinetics of egg activation; PKC stimulators activate the eggs at a significantly enhanced rate ( P < 0.01) compared with activation by calcium ionophore. We show here that PKC stimulators induce emission of the second polar body, but that subsequently, with longer culture, the emitted polar body is absorbed. Our results suggest that the rise in [Ca 2+ ] i serves two functions, to activate PKC and to induce the transition from metaphase II to anaphase II. PKC, once activated, mediates several other events of egg activation.

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PANDA: PAN Cancer Data Analysis Web Tool

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Journal of molecular biology 2025年 169158页

作者： Pepe, G. Notturno Granieri, C. Appierdo, R. Ausiello, G. Helmer-Citterich, M. Gherardini, P.F. Department of Biology University of Rome Tor Vergata Via della Ricerca Scientifica 1 Rome 00133 Italy PhD Program in Cellular and Molecular Biology Department of Biology University of Rome “Tor Vergata” Rome Italy

Cancer research faces challenges due to the genetic diversity within tumors and individual variability. Precision medicine aims to identify genomic and molecular factors linked to clinical outcomes, leveraging large datasets for drug discovery and patient stratification. We introduce PANDA (PAN-cancer Data Analysis web tool) (https://***), a web server designed for analyzing TCGA genomic data. A total of 32 tumor types and 10,711 samples were selected for this analysis. PANDA simplifies complex tasks such as differential expression, survival analysis, and patient stratification, incorporating clinical factors like sex, stage, and treatment history. It also enables the exploration of biological pathways and immune cell type proportion, providing insights into tumor progression. PANDA is user-friendly, designed for researchers with limited informatics expertise, and supports diverse analyses to advance cancer research. © 2025

关键词： cancer biology cancer genomics immune cell deconvolution pan-cancer analysis TCGA patient stratification

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MorPhiC Consortium: towards functional characterization of all human genes

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Nature 2025年第8050期638卷 351-359页

作者： Adli, Mazhar Przybyla, Laralynne Burdett, Tony Burridge, Paul W. Cacheiro, Pilar Chang, Howard Y. Engreitz, Jesse M. Gilbert, Luke A. Greenleaf, William J. Hsu, Li Huangfu, Danwei Hung, Ling-Hong Kundaje, Anshul Li, Shuzhao Parkinson, Helen Qiu, Xiaojie Robson, Paul Schürer, Stephan C. Shojaie, Ali Skarnes, William C. Smedley, Damian Studer, Lorenz Sun, Wei Vidović, Dušica Vierbuchen, Thomas White, Brian S. Yeung, Ka Yee Yue, Feng Zhou, Ting Žurauskienė, Justina Zhong, Aaron Zheng, Shujian Zhao, Hengqiang Zhang, Nan Zhang, Zhehao Zhang, Stephen Zeng, Tony Yu, Bo Yordanova, Galabina N. Yang, Dapeng Xing, De Wang, Xianming Wang, Ping Torre, Denis Tang, Wenzhuo Shivalikanjli, Anu Sengupta, Kaustav Seker, Fidan Ventura, Enrique Sapena Ross, Nicolette C. Rivera-Diaz, Jamilex Rana, Arushi Pongpamorn, Praeploy Poirion, Olivier B. Pillai, Ajay Pilarczyk, Marcin Parker, Devon Ning, Gang Neyisci, Ozlem Nasam, Niharika Mittal, Varun Mitchell, Joshua M. Metzl-Raz, Eyal Meng, Chen Melo-Carrillo, Adrian McDonough, Justin A. Marengo, Gabriel Mao, Yuzhen Leite, Davi Lyra Luo, Renhe Liu, Nianping Liu, Dingyu Liu, Zukai Liu, Si Li, Zhaoheng Kraft, Katerina Koci, Orges A. Kirsammer, Gina Kendra, Angelina Hutter, Carolyn Huebner, Aaron J. Huang, Yung-Hsin Hu, Nan Gupta, Dipayan Gupta, Revant Guo, Tingfeng Griffiths, Alexandra M. Goyal, Juhee Glenn, Rachel A. Garofalo, Jessica L. Fukuda, Bryce Nobutoshi Fu, Yihao Flynn, William F. Flores, Jesse Fletcher, Colin F. Fleming, Patrick J. Felsenfeld, Adam L. Eraslan, Basak Doty, Anthony Dahlstrom, Thomas J. Chung, Caty E. Choudhary, Anshul Cho, Hyein S. Chen, Xintong Chen, Sijie Chan, Chia Baroch, Jacob J. Baker, Dylan S. Bai, Tao Avireddy, Rohan N. V. S. R. K. Amiri, Anahita Diniz, Juliana Alcoforado Abbaszadeh, Neda Robert H. Lurie Comprehensive Cancer Center Department of Obstetrics and Gynecology Northwestern University Feinberg School of Medicine Chicago IL United States Department of Biochemistry and Biophysics University of California San Francisco CA United States Omics Section European Bioinformatics Institute (EMBL-EBI) European Molecular Biology Laboratory Hinxton United Kingdom Department of Pharmacology Center for Pharmacogenomics Northwestern University Feinberg School of Medicine Evanston IL United States William Harvey Research Institute Clinical Pharmacology and Precision Medicine Queen Mary University of London London United Kingdom Department of Dermatology Stanford University Stanford CA United States Department of Genetics Stanford University Stanford CA United States Basic Science and Engineering (BASE) Initiative Stanford University Stanford CA United States Department of Urology University of California San Francisco CA United States Department of Biostatistics Public Health Sciences Fred Hutchinson Cancer Center Seattle WA United States Developmental Biology Program Sloan Kettering Institute New York NY USA School of Engineering and Technology University of Washington Tacoma Tacoma WA United States Departments of Genetics and Computer Science Stanford University Stanford CA United States Jackson Laboratory for Genomic Medicine Farmington CT United States Knowledge Management Section European Bioinformatics Institute (EMBL-EBI) European Molecular Biology Laboratory Hinxton United Kingdom Molecular and Cellular Pharmacology Sylvester Comprehensive Cancer Center University of Miami Coral Gables FL USA Department of Biostatistics University of Washington Seattle WA United States Department of Biochemistry and Molecular Genetics Robert H. Lurie Comprehensive Cancer Center Northwestern University Feinberg School of Medicine Chicago IL United States

Recent advances in functional genomics and human cellular models have substantially enhanced our understanding of the structure and regulation of the human genome. However, our grasp of the molecular functions of human genes remains incomplete and biased towards specific gene classes. The molecular Phenotypes of Null Alleles in Cells (MorPhiC) Consortium aims to address this gap by creating a comprehensive catalogue of the molecular and cellular phenotypes associated with null alleles of all human genes using in vitro multicellular systems. In this Perspective, we present the strategic vision of the MorPhiC Consortium and discuss various strategies for generating null alleles, as well as the challenges involved. We describe the cellular models and scalable phenotypic readouts that will be used in the consortium's initial phase, focusing on 1,000 protein-coding genes. The resulting molecular and cellular data will be compiled into a catalogue of null-allele phenotypes. The methodologies developed in this phase will establish best practices for extending these approaches to all human protein-coding genes. The resources generated-including engineered cell lines, plasmids, phenotypic data, genomic information and computational tools-will be made available to the broader research community to facilitate deeper insights into human gene functions. © 2025. Springer Nature Limited.

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Sugar and metabolic regulation of genes for sucrose metabolism: Potential influence of maize sucrose synthase and soluble invertase responses on carbon partitioning and sugar sensing

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JOURNAL OF EXPERIMENTAL BOTANY 1996年第SPECIAL_ISSUE期47卷 1179-1185页

作者： Koch, KE Wu, Y Xu, J Plant Molecular and Cellular Biology Program Horticultural Sciences Department University of Florida Gainesville FL 32611 USA

Sugar responsiveness of genes for both paths of sucrose metabolism could provide a mechanism not only for transcriptional regulation of the first step in the use of imported carbon, but also for altering signals to the sugar-sensing system. This hypothesis was examined by comparison of (1) sugar regulation among maize genes for sucrose synthase and invertase, (2) their contrasting patterns of tissue expression, and (3) their influence on production of effecters for other sugar-responsive genes. Cloning and characterization of the lvr1 and lvr2 invertase genes of maize indicated that these genes belong to distinct subfamilies of the maize soluble invertase gene family. In addition, maize invertases can be grouped with the sucrose synthases (Sh1 and Sus1) on the basis of shared patterns of differential sugar-responsiveness and tissue-specific expression. Extension of this comparison to include genes for sucrose metabolism from other species revealed a more widespread association between starvation-tolerant expression and restricted patterns of tissue distribution. Consideration of current models for plant sugar-sensing systems and transport pathways suggested that the site and mechanism of sucrose cleavage in the cell could affect the magnitude and type of signal generated.

关键词： carbohydrate regulated genes catabolite repression gene expression hexokinase starvation

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Carbohydrate-modulated gene expression in plants

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ANNUAL REVIEW OF PLANT PHYSIOLOGY AND PLANT molecular biology 1996年第1期47卷 509-540页

作者： Koch, KE Plant Molecular and Cellular Biology Program Horticultural Sciences Department University of Florida Gainesville Florida 32611.

Plant gene responses to changing carbohydrate status can vary markedly. Some genes are induced, some are repressed, and others are minimally affected. As in microorganisms, sugar-sensitive plant genes are part of an ancient system of cellular adjustment to critical nutrient availability. However, in multicellular plants, sugar-regulated expression also provides a mechanism for control of resource distribution among tissues and organs. Carbohydrate depletion upregulates genes for photosynthesis, remobilization, and export, while decreasing mRNAs for storage and utilization. Abundant sugar levels exert opposite effects through a combination of gene repression and induction. Long-term changes in metabolic activity, resource partitioning, and plant form result. Sensitivity of carbohydrate-responsive gene expression to environmental and developmental signals further enhances its potential to aid acclimation. The review addresses the above from molecular to whole-plant levels and considers emerging models for sensing and transducing carbohydrate signals to responsive genes.

关键词： catabolite repression metabolite-regulated genes photosynthate partitioning source/sink relations sucrose

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A pancreatic player in dementia:pathological role for islet amyloid polypeptide accumulation in the brain

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Neural Regeneration Research 2023年第10期18卷 2141-2146页

作者： Angelina S.Bortoletto Ronald J.Parchem Center for Cell and Gene Therapy Stem Cell and Regenerative Medicine CenterDepartment of NeuroscienceDepartment of Molecular and Cellular BiologyTranslational Biology and Molecular Medicine ProgramMedical Scientist Training ProgramBaylor College of MedicineHoustonTXUSA

Type 2 diabetes mellitus patients have a markedly higher risk of developing *** multiple factors contribute to this predisposition,one of these involves the increased secretion of amylin,or islet amyloid polypeptide,that accompanies the pathophysiology of type 2 diabetes *** amyloid polypeptide accumulation has undoubtedly been implicated in various forms of dementia,including Alzheimer’s disease and vascular dementia,but the exact mechanisms underlying islet amyloid polypeptide’s causative role in dementia are *** this review,we have summarized the literature supporting the various mechanisms by which islet amyloid polypeptide accumulation may cause neuronal damage,ultimately leading to the clinical symptoms of *** discuss the evidence for islet amyloid polypeptide deposition in the brain,islet amyloid polypeptide interaction with other amyloids implicated in neurodegeneration,neuroinflammation caused by islet amyloid polypeptide deposition,vascular damage induced by islet amyloid polypeptide accumulation,and islet amyloid polypeptide-induced *** are very few therapies approved for the treatment of dementia,and of these,clinical responses have been controversial at ***,investigating new,targetable pathways is vital for identifying novel therapeutic strategies for treating *** such,we conclude this review by discussing islet amyloid polypeptide accumulation as a potential therapeutic target not only in treating type 2 diabetes mellitus but as a future target in treating or even preventing dementia associated with type 2 diabetes mellitus.

关键词： Alzheimer’s disease amylin amyloid dementia diabetes human islet amyloid polypeptide islet amyloid polypeptide protofibrils type 2 diabetes mellitus vascular dementia

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