Advances in Biological Functions of STAT3 2.0
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".
Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 11668
Special Issue Editor
Interests: targeting STAT3 in cancer; STAT3 GOF mutations; STAT1/3 and chemoradioresistance; role of viruses e.g. HPV and HCV in cancer; IFN/STAT1 and viral immune-evasion; targeting HPV-mediated cancers; CMV and STAT1/3, STAT3/1 in immune modulation in cancers
Special Issue Information
Dear Colleagues,
Since its discovery in the 1990s, acute-phase response factor (APRF), or signal transducer and activator of transcription (STAT) 3, has been shown to perform vital functions at cellular and organellar levels, both under normal as well as stressed conditions. A large amount of information on the regulation of STAT3 function, e.g., its various post-transitional modifications, including its phosphorylation at Tyr705 (pY) and Serine727 (pS) as well as acetylation, methylation, ubiquitination, ISGylation, and SUMOylation, is available now. Apart from its classic canonical phosphorylation-dependent signal transduction and activation pathways, STAT3 is now known to function as a transcription factor even without phosphorylation. Also, in addition to the nucleus, it is now known to reside in the mitochondria as well as in the endoplasmic reticulum.
The generation of cell-specific STAT3 knockout mice has indicated STAT3 contributions to cell- and organ-specific development, e.g., the development of innate immunity, the commitment of common lymphoid (CLP) and myeloid (CMP) progenitors to the dendritic cell (DC) lineage during haematopoiesis, the development of neuronal cells, musculoskeletal system, liver, reproductive tissue, mammary glands, etc. Its largely homeostatic role in various cellular stress conditions, e.g., radiation, oxidative stress, genotoxic stress, cellular senescence, autophagy, ischemia and reperfusion, and hyperosmotic stress, has now been well studied. Apart from its transcriptional functions, various non-transcriptional structural roles of STAT3, e.g., its scaffold function in platelets and its role in cytoskeletal organization, are now also known.
Many of these functions are adaptive, when dysregulated, causes chronic inflammation leading to pathologies, such as cachexia, fibrosis, organ dysfunction, and cancer. The facts that STAT3 is aberrantly activated in 50–100% cases of more than 25 different tumor types, that gain-of-function mutations of STAT3 in leukemia, lymphoma, and adenoma are now reported, and that this overactivated STAT3 plays a role in almost all hallmark functions of cancer cells make it an ideal candidate for drug targeting.
This Special Issue of the International Journal of Molecular Sciences entitled “Advances in Biological Functions of STAT3 2.0” will focus on recent advances in any of the above aspects of STAT3 functions and signal transduction research, e.g., STAT3 deletants and mutants, various organ-specific functions of STAT3, such as STAT3 role in hematopoietic cells, neuronal, or cardiovascular cells, STAT3 functions under normal conditions, STAT3 functions under stress, and regulation of STAT3 function, stressing not only p705- but also pS727-mediated functions, non-canonical functions of STAT3, unphosphorylated STAT3, STAT3 role in immune dysregulation in cancer, and its role in non-cancer diseases, e.g., asthma, inflammatory bowel disease, fibrosis, and metabolic disorders. Contributions on these and any other related topic are welcome.
Dr. Uddalak Bharadwaj
Guest Editor
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Keywords
- STAT3 signaling and its regulation
- STAT3 and development
- STAT3 and fibrosis/cachexia/IBD/cachexia
- STAT3 and metabolism
- STAT3 functions under stress
- Non-canonical functions of STAT3
- STAT3 GOF and LOF mutants
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