Cited by 36Immunodeficiency and Autoimmune DisordersCytokine Signaling Pathways and InteractionsT-cell and B-cell Immunology

Protein stabilization improves STAT3 function in autosomal dominant hyper-IgE syndrome

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Bocchini, Claire E., Nahmod, Karen, Katsonis, Panagiotis, Kim, Sang, Kasembeli, Moses M., Freeman, Alexandra, Lichtarge, Olivier, Makedonas, George +1 more·2016·Blood

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Authors
Bocchini, C. E., Nahmod, K., Katsonis, P., Kim, S., Kasembeli, M. M., Freeman, A., Lichtarge, O., Makedonas, G., & Tweardy, D. J.
Affiliations
  • Department of Pediatrics and
  • Baylor College of Medicine (US)
  • The University of Texas MD Anderson Cancer Center (US)
  • National Institutes of Health (US)
Venue
Blood
Published
2016-12-29
Volume
128
Issue
26
Pages
3061-3072
ISSN
  • 0006-4971 (ISSN-L)
  • 1528-0020
OpenAlex
W2542557406
Cited by
36
References
3
Citations by year
2026: 1 · 2025: 4 · 2024: 2 · 2023: 3 · 2022: 4 · 2021: 2 · 2020: 4 · 2019: 9 · 2018: 5 · 2017: 1 · 2016: 1
FWCI
3.23
Type
journal article
Language
en
Open access
Locations
  • Blood (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Science Foundation (1062455, 0905536)
  • Sanofi
  • Texas Children's Hospital
  • Rice University
  • National Institutes of Health (1pn1ey016525-01, PN1EY016525, GM66099)
  • Sanofi Pasteur
  • National Eye Institute ((PN1 EY016525)
  • National Institute of General Medical Sciences (R01GM066099, R01GM079656)
  • National Institute of Child Health and Human Development
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (K12HD041648)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
autosomal dominant hyper-IgE syndrome, STAT3, protein stabilization, molecular chaperones, STAT3 mutations, T cells, splenocytes, protein stability, therapeutic target
MeSH terms
Heat Shock Transcription Factors, Animals, Diterpenes, DNA-Binding Proteins, Herpesvirus 4, Human, Half-Life, Humans, Job Syndrome, Models, Molecular, Mutation, Protein Binding, Spleen, Transcription Factors, CD4-Positive T-Lymphocytes, Cytokines, CD8-Positive T-Lymphocytes, Phosphotyrosine, Interleukin-17, Mutant Proteins, STAT3 Transcription Factor, Mice, Protein Stability

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