جستجوی استاد راهنمای دانشگاهی

Silvia Santos is a Group Leader at the Francis Crick Institute, leading the Quantitative Stem Cell Biology Lab since January 2018. Her research focuses on understanding cell decision-making during transitions, specifically cell division and differentiation in early development using human embryonic stem cells. She combines experimental techniques with theoretical approaches, including advanced microscopy, genomics, and computational modeling. Education and Career: PhD in Molecular and Cell Biology from EMBL-Heidelberg (2008), followed by postdoctoral training at Stanford University (2009-2014). She held an MRC Career Development Award at Imperial College London (2014-2017) before joining the Crick. Her work emphasizes interdisciplinary methods to study cellular processes in health and disease. Research Interests: Spatial-temporal control in cell decisions, stem cell differentiation, cell cycle regulation, and modeling embryonic development. She advocates for women in science and mentorship programs for early-career researchers. Key Achievements: Recipient of Marie Curie E-Star, EMBO, and HFSP fellowships. Recognized with the BioModels’ Model of the Year 2023 for contributions to systems biology. Her lab develops models like gastruloids to study embryonic development. Grants and Mentorship: Supported by MRC and other grants. Committed to fostering excellence in training and mentorship, previously chairing mentorship initiatives at Imperial College London. Labs and Teams: Quantitative Stem Cell Biology Lab at the Crick, collaborating with interdisciplinary teams on projects involving proteomics, genomics, and high-throughput screening.

• Developmental Biology
• Cell Biology
• Cell Cycle & Chromosomes
• +۳ مورد دیگر

John Diffley is a Principal Group Leader and Associate Research Director at The Francis Crick Institute in London, UK, where he leads research on DNA replication mechanisms. His work focuses on understanding how cells precisely duplicate their DNA during cell division and how errors in this process contribute to cancer development. Diffley obtained his PhD from New York University in 1985 and completed postdoctoral training with Bruce Stillman at Cold Spring Harbor Laboratory until 1990. He established his research group at the Clare Hall Laboratories (originally Imperial Cancer Research Fund, then Cancer Research UK) before moving to The Francis Crick Institute in 2015. His research spans DNA replication initiation, cell cycle control, replication fork checkpoints, and epigenetic inheritance. Diffley's lab has pioneered methods to reconstitute chromatin replication using purified proteins, providing unprecedented insights into chromosome biology. His team combines genetics, cell biology, and biochemistry to study the molecular 'machines' that copy DNA in yeast and human cells. Analysis of Diffley's recent publications reveals a strong focus on structural mechanisms of DNA replication, particularly using cryo-EM to visualize replication machinery. His work examines helicase loading and activation, replication fork stability under stress, and the connection between replication errors and cancer development. The research spans model organisms to human cells, with increasing emphasis on structural approaches in recent years. FRS (Fellow of the Royal Society) FMedSci (Fellow of the Academy of Medical Sciences) Diffley actively mentors a diverse team of postdoctoral researchers and PhD students, investigating various aspects of DNA replication. His lab has received substantial funding to support their work on replication mechanisms, with projects spanning basic biochemical reconstitution to studies of replication errors in cancer contexts. The lab maintains multiple technical platforms including structural biology, biochemistry, and cell biology approaches. His research group operates within The Francis Crick Institute's collaborative environment, utilizing shared facilities for structural biology, microscopy, and genomics to advance understanding of DNA replication mechanisms and their implications for genome stability and disease.

• DNA Replication
• Cell Cycle Control
• Chromosome Biology
• +۵ مورد دیگر

Hajime Murakami is an Advanced Research Fellow at the University of Aberdeen's School of Medicine, Medical Sciences and Nutrition, where he conducts cutting-edge research on meiotic recombination mechanisms. His work focuses on understanding how cells manage the complex process of DNA double-strand break formation and repair during meiosis, with implications for human fertility and chromosome disorders. Dr. Murakami's research interests center on the molecular mechanisms of meiotic recombination, particularly the role of DNA double-strand breaks (DSBs) in chromosome segregation. His laboratory investigates how proteins like Hop1 and Red1 function as 'manager proteins' that direct the DNA 'scissors' to appropriate chromosomal locations, ensuring proper recombination while preventing errors that could lead to miscarriage or congenital syndromes. His work primarily uses yeast as a model system, which shares fundamental meiotic mechanisms with humans. Analysis of Dr. Murakami's publication record reveals a consistent focus on the molecular regulation of meiotic recombination across his career. His research has progressively uncovered sophisticated control mechanisms that ensure accurate chromosome segregation, with particular emphasis on how cells manage DNA break formation across chromosomes of different sizes. His work spans fundamental molecular mechanisms to potential clinical applications in reproductive medicine. Dr. Murakami has received significant recognition for his work, most notably a Medical Research Council (MRC) Career Development Award, which supports his ongoing research into the molecular basis of meiotic recombination. As an active researcher accepting PhD students in Biomedical Sciences, Dr. Murakami continues to advance our understanding of fundamental genetic processes that underlie human reproductive health. His laboratory at the Institute of Medical Sciences on Foresterhill Campus employs yeast genetics and molecular biology approaches to investigate the critical processes that ensure proper chromosome segregation during gamete formation.

• Genetics
• Genomics
• Molecular Biology
• +۳ مورد دیگر

Dr Michael Boemo is an Assistant Professor at the University of Cambridge, holding dual appointments in the Department of Pathology and Department of Genetics. He leads research at the intersection of computational biology, DNA replication, and cancer genomics, developing machine learning tools to analyze replication stress and genomic instability. Academic Background: BA in Mathematics (Rutgers University), PhD in Physics (University of Oxford) Research Focus: Genomic instability in cancer, DNA replication/repair defects, computational modeling using machine learning and high-performance simulations Teaching: Lectures in Natural Sciences Tripos (mathematical biology, genetics, systems biology), module organizer for cancer biology and biological modeling His research group leverages nanopore sequencing and AI to map replication fork dynamics, revealing how stalled forks generate mutations in cancer cells and pathogens. Recent work examines extrachromosomal DNA replication vulnerabilities and transcription-replication conflicts. Dr Boemo collaborates across computational biology and cancer research domains, with publications spanning journals like Nature Methods, Cell, and PLoS Computational Biology. His lab develops tools such as DNAscent for replication fork analysis and explores therapeutic targeting of replication stress.

• Genomic Instability
• DNA Replication and Repair
• Computational Biology
• +۵ مورد دیگر

Professor Tomoyuki Tanaka holds the Chair of Cell and Molecular Biology at the University of Dundee within the School of Life Sciences . He serves as the Academic Lead of Dundee Imaging Facility (since 2018) and Deputy Head of the Division for Molecular Cell & Developmental Biology (since 2022). His research focuses on chromosome segregation mechanisms in mitosis and their implications in genetic diseases and cancer . Member of European Molecular Biology Organisation (EMBO, 2008–) Fellow of Royal Society of Edinburgh (2009–) Wellcome Trust Investigator (2020–) His lab investigates two key processes in early mitosis: chromosome reorganization (resolution and compaction of sister chromatids) and kinetochore-spindle interactions . These mechanisms are critical for preventing errors linked to aneuploidy, congenital disorders, and cancers . Using budding yeast as a model organism, his group combines genetic, proteomic, and imaging techniques to uncover conserved biological principles. Recent publications highlight discoveries in condensin exclusion during prophase , Aurora B kinase spatial regulation , and error correction mechanisms for accurate chromosome inheritance. The lab also contributes to in vitro reconstitution of chromosomal processes, including a 2021 breakthrough on chromosome positioning networks . 2020: Wellcome Investigator Award 2013: ERC Advanced Grant 2007: Hooke Medal (British Society for Cell Biology) 2000: EMBO Young Investigator He supervises PhD students and contributes to Level 3 undergraduate teaching (BS31006 Gene Regulation) and Honours research projects . His work aligns with UN Sustainable Development Goals for health and well-being through genetic disease research.

• Chromosome Segregation
• Mitosis
• Cell Cycle Regulation
• +۷ مورد دیگر

J. Ross Chapman is a Professor of Genome Maintenance Biology at the University of Oxford, affiliated with the MRC Molecular Haematology Unit. He holds fellowships from Cancer Research UK and the Lister Institute, and is part of the EMBO Young Investigator Programme. His research focuses on DNA repair mechanisms, particularly the balance between accurate and mutagenic repair pathways in cancer and immune disorders. Career highlights include roles as a Sir Henry Wellcome Fellow and Principal Investigator. His group studies genetic recombination mechanisms, aiming to develop cancer therapies targeting repair pathway dysfunctions. Key research areas include the role of BRCA1, BARD1, 53BP1, and CST complexes in DNA repair. Awards include CRUK and Lister Institute Fellowships, alongside EMBO recognition. His lab’s work spans genomic stability, immune system development, and cancer therapy strategies. Recent studies explore chronic inflammation in leukemia evolution and synthetic lethality in BRCA-deficient cells.

• Genome Stability
• DNA Repair Mechanisms
• Cancer Biology
• +۳ مورد دیگر

John Rouse is a Professor and Scientific Programme Leader (MRC) of Chromosome Biology at the MRC PPU. His research focuses on DNA repair mechanisms, chromatin structure, and genome maintenance. He leads projects funded by the Medical Research Council (MRC) and other institutions, including collaborative efforts on chromatin remodelling and DNA interstrand crosslink repair. Key roles: MRC QQR Programme Leader (2018–2024), Investigator on multiple collaborative grants. Research interests: Chromosome biology, DNA damage response, histone chaperones, and kinase signaling pathways. His work contributes to understanding genome integrity and has implications for cancer therapy and neurodegenerative diseases. Notable projects include the study of NEK1 kinase in ALS and the development of targeted cancer therapies using PROTAC technology. John has been involved in public engagement activities, such as the Discovery Days 2012 event, promoting science outreach.

• DNA Damage
• DNA Repair
• Chromatin Structure
• +۵ مورد دیگر

Simon Boulton is a distinguished molecular biologist and cancer researcher serving as a Senior Group Leader at the Francis Crick Institute and holding an honorary Professorship at University College London. He also serves as Senior Vice President of Science Strategy at Artios Pharma Ltd, which he helped establish in 2016, where he additionally chairs the Scientific Advisory Board and serves on the Executive Board. His educational background includes: Molecular Biology studies at the University of Edinburgh PhD at the University of Cambridge with Professor Steve Jackson (Gurdon Institute) EMBO and HFSP funded postdoctoral fellowships at Harvard Medical School with Prof. Nick Dyson (MGH Cancer Centre) and Prof. Marc Vidal (Dana Farber Cancer Institute) Boulton's research focuses on understanding DNA damage response mechanisms, particularly DNA double-strand break repair in both mitotic and meiotic cells. His laboratory employs the complementary experimental strengths of C. elegans and mouse genetics, combined with cell biology and biochemistry approaches. Over his career, his lab has discovered novel DNA repair genes and provided crucial molecular insights into human diseases, especially cancer. His work bridges fundamental biological processes with potential therapeutic applications in oncology. Analysis of his recent publications reveals a consistent focus on genome integrity mechanisms, with particular emphasis on DNA repair pathways, telomere biology, replication stress responses, and the development of novel assays to study these processes. His research increasingly intersects with cancer therapeutics, particularly through his work with Artios Pharma on DNA Damage Response (DDR) target pipelines. His significant scientific contributions have been recognized with numerous prestigious awards: Member of EMBO Fellowship of the Academy of Medical Sciences Colworth Medal European Association for Cancer Research (EACR) Young Investigator Award Eppendorf/Nature Award for Young European Investigators Royal Society Wolfson Research Merit award EMBO Gold Medal Paul Marks Prize for Cancer Research Royal Society Francis Crick Prize lecture Mendel Lecture Boulton has secured substantial research funding throughout his career, including EMBO and HFSP postdoctoral fellowships, and currently leads a well-funded research group at the Crick Institute. His dual role in academia and industry through Artios Pharma demonstrates a successful translation of basic research into therapeutic development, with the company building an innovative DNA Damage Response (DDR) target pipeline aimed at transforming cancer therapy. His laboratory at the Francis Crick Institute maintains strong collaborative networks across multiple disciplines, utilizing advanced facilities including proteomics, genomics, bioinformatics, and microscopy resources. The lab's work spans from fundamental DNA repair mechanisms to potential clinical applications, with a particular focus on how failures in DNA repair contribute to cancer and other diseases.

• DNA Damage Response
• DNA Repair
• Genome Integrity & Repair
• +۷ مورد دیگر

J. Ross Chapman is a Professor of Genome Maintenance Biology at the University of Oxford, holding positions at the MRC Molecular Haematology Unit (part of the Radcliffe Department of Medicine) and the Wellcome Centre for Human Genetics. He is a Cancer Research UK (CRUK) Career Development Fellow, Lister Institute Research Fellow, and EMBO Young Investigator Programme member. His research focuses on DNA repair mechanisms, particularly the balance between accurate and mutagenic repair pathways in cancer and immune systems. Key affiliations include the Francis Crick Institute and previous roles at the University of Sussex and Gurdon Institute. Education and Career Path: Started as a Research Assistant at the MRC Genome Damage and Stability Centre (2002), earned his PhD in Steve Jackson’s lab (2006), and held postdoctoral roles at Simon Boulton’s lab (2010). Established his independent group at Oxford in 2013, becoming an Associate Professor in 2017 and moving to the MRC Unit in 2020. Research Interests: Investigates genetic recombination mechanisms, DNA double-strand break (DSB) repair pathways, and their roles in immune system development and cancer. Recent work explores how faulty repair mechanisms drive cancer and immune disorders, targeting vulnerabilities for therapies like PARP inhibitors. Publications: Recent studies include discoveries on Shieldin/CST complex roles in DNA repair, BLM-BRCA1 interactions, and chronic inflammation in leukemia. His work bridges basic biology with clinical applications, such as drug resistance mechanisms in BRCA-deficient cancers. Awards: CRUK CDF, Lister Fellowship, EMBO Young Investigator Programme membership, and recognition for contributions to DNA repair research. Lab Team: Includes postdoctoral researchers (e.g., Ashleigh King, My Khanh Pham), DPhil students, and technical staff. Collaborates on projects like PARP inhibitor efficacy and immune system DNA repair dynamics.

• DNA Repair Mechanisms
• Cancer Biology
• Genome Stability
• +۳ مورد دیگر

Dr. Suzanne Madgwick is a Researcher at Newcastle University, focusing on reproductive and developmental biology with a strong emphasis on oocyte biology, meiotic regulation, and fertility mechanisms. Her work bridges molecular, cellular, and organismal levels to understand fundamental processes in reproduction. She has collaborated extensively with colleagues such as Dr. Mark Levasseur and Dr. David Bulmer, contributing to advancements in understanding chromosome segregation, cell cycle control, and fertility disorders. Her research interests include meiotic arrest mechanisms, cyclin-CDK signaling pathways, and the molecular basis of aneuploidy prevention in oocytes. She has also explored topics such as egg activation, calmodulin-dependent signaling, and the role of specific proteins like separase and Emi2 in reproductive processes. Additionally, her recent work addresses broader scientific community challenges, including promoting inclusivity and sustainability in scientific meetings. Dr. Madgwick’s publications span over two decades, reflecting her sustained contributions to reproductive and cell biology. Her experimental approaches often involve mouse models to study developmental and genetic mechanisms. Despite her extensive research output, she has not explicitly listed student advisees or major grants in the provided text. She is affiliated with Newcastle University’s research groups focused on reproductive science and developmental biology.

• Reproductive Biology
• Cell Biology
• Molecular Biology
• +۳ مورد دیگر

Dr. Marta Shahbazi is an Affiliated Principal Investigator at the Cambridge Stem Cell Institute, University of Cambridge, and maintains a primary affiliation with the MRC Laboratory of Molecular Biology. She leads the Shahbazi Lab, which focuses on understanding the mechanisms that control pluripotent stem cell identity and fate in physiological 3D contexts. Her research bridges developmental biology and stem cell research, with particular emphasis on how tissue architecture influences stem cell behavior during embryonic development and potential regenerative applications. Dr. Shahbazi's research interests center around pluripotent stem cells and their role in early mammalian development. Her work investigates how pluripotent cells undergo concomitant changes in shape and identity to establish the foundation of the body plan. She is particularly interested in epithelial tissue determinants and their contribution to stem cell fate decisions. Her lab employs novel methods to culture mouse and human embryos, 3D embryonic stem cell models, and adult tissue organoids to understand the molecular pathways coordinating tissue shape and stem cell fate during pluripotency exit and acquisition. Analysis of Dr. Shahbazi's recent publications reveals a strong focus on human and mouse embryogenesis, with particular attention to tissue morphogenesis, cell delamination, and the molecular mechanisms underlying pluripotency transitions. Her work spans from basic developmental mechanisms to potential applications in regenerative medicine, with increasing emphasis on human embryo models in recent years. The research demonstrates interdisciplinary approaches combining cell biology, developmental biology, and tissue engineering principles. Dr. Shahbazi has received recognition through multiple publications in high-impact journals including Nature, Developmental Cell, and Cell Stem Cell. Her work on human embryo development and stem cell-based embryo models has contributed significantly to the field. Dr. Shahbazi mentors several researchers in her lab, including Viviane de Souza Rosa, Miguel Ángel Ortiz Salazar, Rina Sakata, Nanami Satoh, Luca Schwarz, and Anfu Wang. Her research is supported by the Cambridge Stem Cell Institute and the MRC Laboratory of Molecular Biology, providing resources for advanced imaging, genomics, and tissue culture facilities. The Shahbazi Lab is part of the broader Cambridge research ecosystem focused on stem cells and developmental biology, collaborating with other principal investigators at the Cambridge Stem Cell Institute.

• Developmental Biology
• Stem Cell Biology
• Embryogenesis
• +۴ مورد دیگر

Munira Kadhim is a Professor in Radiation Biology at the School of Biological and Medical Sciences, Oxford Brookes University. She holds a PhD in Genetics from Swansea University and has previously worked at Swansea University, the Weatherall Institute of Molecular Medicine (University of Oxford), and the Medical Research Council (Harwell) as a research group leader for Genomic Instability. First degree in Biology from Baghdad University PhD in Genetics from Swansea University Her research focuses on non-targeted effects of radiation, including genomic instability and bystander effects, with significant conceptual impact on dose limit recommendations in clinical and environmental contexts. She has advised UK Government Departments via COMARE and contributed to new clinical guidelines for low-dose radiation usage such as CT scans. Her recent publications explore radiation-induced cellular communication, exosome-mediated damage propagation, and miRNA roles in stress responses. Research spans direct and indirect radiation effects on mammalian cells, including bone marrow, lymphocytes, and cancer cells, using chromosome analysis and DNA damage techniques. Professor Kadhim teaches Biomedical Science (BSc) and Medical Genetics and Genomics (MSc) courses, covering modules in biotechnology, evidence-based medicine, and cellular signaling. She leads the Radiation Biology research group and is principal investigator for the DISCOVER project (2024-2026), funded by the European Commission.

• Radiation Biology
• Genomic Instability
• Bystander Effects
• +۴ مورد دیگر

Dr. Stephanie Meyer is a Researcher at Newcastle University, focusing on interdisciplinary research in toxicology, molecular biology, and environmental health. Her work spans investigations into chemical toxicity, cellular mechanisms in mitosis, and the effects of environmental and pharmaceutical agents on liver function. She collaborates extensively with academic and industry partners, contributing to advancements in in vitro hepatocyte models for drug safety testing and studies on endocrine disruptors. Her research interests include hepatotoxicity, epigenetic regulation, and radiation biology. Recent studies highlight her exploration of ionic liquid toxicity, estrogen receptor interactions, and the development of novel biotechnological tools like the NanoBiT luciferase system. Dr. Meyer also addresses public health policy through analyses of patent law reforms affecting medicine accessibility in South Africa. Key contributions include identifying xenobiotic triggers in autoimmune liver diseases and establishing B-13/H cell models for lipid dysregulation studies. Her work bridges basic science and applied toxicology, with implications for regulatory safety assessments and clinical practices.

• Toxicology
• Molecular Biology
• Hepatology
• +۷ مورد دیگر

Professor Rhona Anderson is a leading academic in Radiation Biology at Brunel University London, affiliated with the Department of Life Sciences under the College of Health, Medicine and Life Sciences . As a Professor and Director of the Centre for Health Effects of Radiological and Chemical Agents , she leads research into the genomic and health impacts of ionizing radiation. Qualifications: PhD, MSc, and BSc (Hons) in life sciences-related fields, with professional certification as a Clinical Cytogeneticist . Research Interests focus on radiation cytogenetics , low-dose radiation effects , and genetic biomarkers of radiation exposure . Her work extends to veterans' health , occupational radiation risks , and mechanisms of DNA damage . Trends in Recent Publications highlight her expertise in chromosome aberration analysis , intergenerational radiation effects , and biomarker development for radiation exposure. Her studies span medical , environmental , and occupational radiation sources , using advanced techniques like M-FISH and germline mutation analysis . Scientific Awards: 2023: Elected Vice-President, International Association for Radiation Research 2017: Honorary Membership, Royal College of Radiology, UK Advising and Grants include leadership of the Centre for Health Effects of Radiological and Chemical Agents and supervision of PhD projects on radiation health risks. While specific grant details are not listed, her extensive publication record reflects sustained research funding. Labs and Teams include the Centre for Health Effects of Radiological and Chemical Agents and collaboration with the IEHS (Institute of Environment, Health and Societies) research group.

• Radiation Biology
• Radiation Cytogenetics
• Low Dose Radiation Research
• +۳ مورد دیگر

Dr. Helen Matthews is a Research Fellow at the University of Sheffield's School of Biosciences, holding the Wellcome Trust/Royal Society Sir Henry Dale Fellowship since 2021. Her research focuses on understanding cell division mechanics in normal tissues and cancer, combining cell biology, microscopy, and biophysical techniques. She investigates how oncogenic signals alter cell shape and mechanics during mitosis, particularly in pancreatic cancer and tumor microenvironments. Matthews earned her MSci from Imperial College London (2000–2004) and a PhD from University College London (2004–2008), advised by Roberto Mayor. Postdoctoral work at the MRC Laboratory for Molecular Cell Biology (2009–2021) under Buzz Baum deepened her expertise in cell division mechanics. She also held visiting roles at Institut Curie (Paris) and the Francis Crick Institute. Her lab employs biophysical tools to study how mechanical forces influence cell division, including microfabrication to mimic tumor stiffness. Key areas include Ras-driven oncogenesis, epithelial tissue mechanics, and mitotic rounding dynamics. Recent work highlights Ras's role in disrupting cell-substrate interactions during division, impacting tumor formation. Awards: Wellcome Trust/Royal Society Sir Henry Dale Fellowship (2021–present) Labs/Teams: Based in the Molecular Cell Biology cluster at Sheffield, focusing on cancer cell mechanics and tumor microenvironment interactions.

• Cell Biology
• Cancer Biology
• Biophysics
• +۳ مورد دیگر