Stephen Μ. Hedrick

ORCID: 0000-0002-6345-8751
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About
Contact & Profiles
Research Areas
  • T-cell and B-cell Immunology
  • Immune Cell Function and Interaction
  • Monoclonal and Polyclonal Antibodies Research
  • Immunotherapy and Immune Responses
  • CAR-T cell therapy research
  • FOXO transcription factor regulation
  • Immune Response and Inflammation
  • Cell death mechanisms and regulation
  • Signaling Pathways in Disease
  • Glycosylation and Glycoproteins Research
  • vaccines and immunoinformatics approaches
  • Phagocytosis and Immune Regulation
  • CRISPR and Genetic Engineering
  • Cytokine Signaling Pathways and Interactions
  • Galectins and Cancer Biology
  • NF-κB Signaling Pathways
  • Ubiquitin and proteasome pathways
  • Cell Adhesion Molecules Research
  • Invertebrate Immune Response Mechanisms
  • Diabetes and associated disorders
  • Melanoma and MAPK Pathways
  • Cancer Immunotherapy and Biomarkers
  • Protein Degradation and Inhibitors
  • Single-cell and spatial transcriptomics
  • Atherosclerosis and Cardiovascular Diseases

University of California, San Diego
2015-2025

Thompson Cancer Survival Center
2024

Canton City School District
2021

Universidad Católica Santo Domingo
2006

The University of Tokyo
2002-2005

University of Shizuoka
2005

Moores Cancer Center
2005

MRC Laboratory of Molecular Biology
2002

Howard Hughes Medical Institute
2002

University of Illinois Urbana-Champaign
1998

A surge of luteinizing hormone (LH) from the pituitary gland triggers ovulation, oocyte maturation, and luteinization for successful reproduction in mammals. Because signaling molecules RAS ERK1/2 (extracellular signal-regulated kinases 1 2) are activated by an LH granulosa cells preovulatory follicles, we disrupted Erk1/2 mouse provide vivo evidence that these necessary LH-induced resumption meiosis, luteinization. In addition, biochemical analyses selected disruption Cebpb gene demonstrate...

10.1126/science.1171396 article EN Science 2009-05-14

The forkhead O transcription factors (FOXO) integrate a range of extracellular signals, including growth factor signaling, inflammation, oxidative stress, and nutrient availability, to substantially alter the program gene expression modulate cell survival, cycle progression, many yet be unraveled type–specific responses. Naive antigen-specific CD8+ T cells undergo rapid expansion arming effector function within days pathogen exposure. In addition, by peak expansion, they form precursors...

10.1084/jem.20130392 article EN cc-by-nc-sa The Journal of Experimental Medicine 2013-05-27

Highlights•ICOS signaling transiently inactivates FOXO1 to generate Tfh cells•FOXO1 regulates a cell gene program exemplified by negative regulation of Bcl6•Enforced nuclear localization prevents differentiation•FOXO1 promotes final GC-Tfh differentiationSummaryT follicular helper (Tfh) cells are essential in the induction high-affinity, class-switched antibodies. The differentiation is multi-step process that depends upon co-receptor ICOS and activation phosphoinositide-3 kinase leading...

10.1016/j.immuni.2015.01.017 article EN cc-by Immunity 2015-02-01

Mechanistic understanding of the inhibitory immunoreceptor PD-1 is largely based on mouse models, but human and share only 59.6% amino acid identity. Here, we found that more than PD-1, owing to stronger interactions with ligands PD-L1 PD-L2 efficient recruitment effector phosphatase Shp2. In a melanoma model adoptively transferred T cells, humanization intracellular domain disrupted antitumor activity CD8

10.1126/sciimmunol.ads6295 article EN Science Immunology 2025-01-03
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