Sankar Ghosh

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Sankar Ghosh
Sankar Ghosh.jpg
Alma mater Albert Einstein College of Medicine (PhD)
Whitehead Institute at MIT (Post-Doctoral Training)
Calcutta University (BSc, MSc)
TitleChair, Department of Microbiology & Immunology at Columbia University Irving Medical Center
AwardsInvestigator, Howard Hughes Medical Institute (1991-2004)
MERIT Award, National Institutes of Health (2001-2011)
AAAI-Pharmigen Investigator Award (2002)
Ranbaxy Science Foundation Award in Basic Medical Research (2006)
F.W. Alt Award for New Discoveries in Immunology (2008)
Outstanding Scientist Award, American Association for Indian Scientists in Cancer Research (2010)
Professor J.J. Ghosh Memorial Award, Calcutta University (2011)
Distinguished Alumni Award, Albert Einstein College of Medicine (2017)
Clarivate Analytics/Web of Science Highly Cited Researcher (1999, 2022)
HonoursFellow, American Association for the Advancement of Sciences (2007)
Member, National Academy of Sciences (2021)
Member, National Academy of Medicine (2022)
Member, American Academy of Arts & Sciences (2023)
Website https://www.sankarghoshlab.org

Sankar Ghosh is an Indian-American immunologist, microbiologist, and biochemist, who is the Chair and Silverstein & Hutt Family Professor of the Department of Microbiology & Immunology at Columbia University Irving Medical Center. [1] Ghosh is best known for his pioneering research on the activation of cellular responses via NF-κB, a transcription factor that plays a critical role in regulating the expression of a large number of genes involved in the mammalian immune system. Ghosh's research led to the first cloning and characterization of NF-κB and IkB proteins, including the demonstration of the role of IkB phosphorylation in the activation of NF-κB.

Contents

Over the years, Ghosh's research has been prominently published in numerous leading scientific journals. Ghosh was elected to the American Academy of Arts & Sciences in 2023, [2] to the National Academy of Medicine in 2022, [3] and the National Academy of Sciences in 2021. [4] He previously was elected a Fellow of the American Association for the Advancement of Science in 2007 for his "distinguished contributions to the field of immunology, particularly for studies of the NF-kB signaling pathway." [5]


Education

Ghosh received his Ph.D. in Molecular Biology from the Albert Einstein College of Medicine in 1988. He then did his postdoctoral research training with Nobel Laureate Dr. David Baltimore at the Whitehead Institute at MIT in Cambridge, MA. Ghosh previously received his B.Sc. and M.Sc. degrees from Calcutta University in India.

While in Baltimore's lab, Dr. Ghosh began his work in understanding the regulation of NF-κB. Ghosh was instrumental in identifying, cloning and characterizing key components of the NF-κB pathway and his research led to the publication of multiple papers in leading scientific journals, including Nature, Cell, and Science.

Career

After his success at the Baltimore lab, Ghosh began his independent research career at Yale University School of Medicine in 1991, serving as a professor in the Departments of Immunobiology and Molecular Biophysics & Biochemistry. At Yale, Ghosh's laboratory made numerous original findings that helped establish the mechanism of transcriptional regulation of NF-κB proteins, identification and characterization of signaling intermediates in innate and adaptive immune system, and identification and characterization of a subset of Toll-like receptors.

At Yale, Ghosh was an Investigator of the Howard Hughes Medical Institute. [6] Ghosh was awarded the 2005 Ranbaxy Research Award in Basic Science. [7] In 2007, Ghosh was named a Fellow of the American Association for the Advancement of Science (AAAS). [8]

In 2008, after 17 years at Yale, Ghosh was recruited to Columbia University and the Columbia University Irving Medical Center to become the Chair of the Department of Microbiology & Immunology. At Columbia, Ghosh continued his lab's pioneering research into NF-κB while broadening the lab's focus to address a wide variety of diseases including rheumatoid arthritis, celiac disease, Alzheimer's disease, sepsis, and cancer. Major research findings by Ghosh at Columbia have included establishing a central role of c-Rel in the suppression of anti-tumor activity, identifying a variant in a non-coding RNA that may contribute to the intestinal inflammation in celiac disease, and identifying specific microRNA biomarkers that potentially indicate a strong likelihood of poor prognosis for sepsis patients.

Dr. Ghosh has served in an advisory capacity for several organizations including the Board of Scientific Counselors of the National Cancer Institute, the Scientific Review Board of the Damon Runyon Cancer Research Foundation and the Scientific Review Council of the Leukemia and Lymphoma Society. He also served as a member of the Board of Management of the National Center for Biological Sciences in Bangalore, India, as well as scientific advisory boards of Center for Life Sciences (CLS) for Peking University and Tsinghua University, Beijing, China, Shanghai Institute of Immunology, Shanghai, China, and Max-Planck Institute, Freiburg, Germany. He has served on the editorial board of multiple journals including Immunity, Molecular and Cellular Biology and the Journal of Biological Chemistry. He also served on the Life Sciences jury for the Infosys Prize in 2011.

Dr. Ghosh has been recognized for his highly cited publications as a Clarivate Analytics/Web of Science Highly Cited Researcher. [9]

In April 2021, Ghosh was elected to the National Academy of Sciences, [4] then in October 2022 to the National Academy of Medicine, [3] and in April 2023 to the American Academy of Arts & Sciences. [2]

Bibliography

Selected publications

Related Research Articles

<span class="mw-page-title-main">NF-κB</span> Family of transcription factor protein complexes

Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is a family of transcription factor protein complexes that controls transcription of DNA, cytokine production and cell survival. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, heavy metals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens. NF-κB plays a key role in regulating the immune response to infection. Incorrect regulation of NF-κB has been linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection, and improper immune development. NF-κB has also been implicated in processes of synaptic plasticity and memory.

<span class="mw-page-title-main">IKBKG</span> Protein-coding gene in the species Homo sapiens

NF-kappa-B essential modulator (NEMO) also known as inhibitor of nuclear factor kappa-B kinase subunit gamma (IKK-γ) is a protein that in humans is encoded by the IKBKG gene. NEMO is a subunit of the IκB kinase complex that activates NF-κB. The human gene for IKBKG is located on the chromosome band Xq28. Multiple transcript variants encoding different isoforms have been found for this gene.

<span class="mw-page-title-main">IKK2</span> Protein-coding gene in the species Homo sapiens

IKK-β also known as inhibitor of nuclear factor kappa-B kinase subunit beta is a protein that in humans is encoded by the IKBKB gene.

<span class="mw-page-title-main">NFKB1</span> Protein-coding gene in the species Homo sapiens

Nuclear factor NF-kappa-B p105 subunit is a protein that in humans is encoded by the NFKB1 gene.

The IκB kinase is an enzyme complex that is involved in propagating the cellular response to inflammation, specifically the regulation of lymphocytes.

<span class="mw-page-title-main">IκBα</span> Protein-coding gene in the species Homo sapiens

IκBα is one member of a family of cellular proteins that function to inhibit the NF-κB transcription factor. IκBα inhibits NF-κB by masking the nuclear localization signals (NLS) of NF-κB proteins and keeping them sequestered in an inactive state in the cytoplasm. In addition, IκBα blocks the ability of NF-κB transcription factors to bind to DNA, which is required for NF-κB's proper functioning.

<span class="mw-page-title-main">RELA</span> Protein-coding gene in the species Homo sapiens

Transcription factor p65 also known as nuclear factor NF-kappa-B p65 subunit is a protein that in humans is encoded by the RELA gene.

<span class="mw-page-title-main">NFKB2</span> Protein-coding gene in the species Homo sapiens

Nuclear factor NF-kappa-B p100 subunit is a protein that in humans is encoded by the NFKB2 gene.

<span class="mw-page-title-main">CHUK</span> Protein-coding gene in humans

Inhibitor of nuclear factor kappa-B kinase subunit alpha (IKK-α) also known as IKK1 or conserved helix-loop-helix ubiquitous kinase (CHUK) is a protein kinase that in humans is encoded by the CHUK gene. IKK-α is part of the IκB kinase complex that plays an important role in regulating the NF-κB transcription factor. However, IKK-α has many additional cellular targets, and is thought to function independently of the NF-κB pathway to regulate epidermal differentiation.

<span class="mw-page-title-main">RELB</span> Protein-coding gene in the species Homo sapiens

Transcription factor RelB is a protein that in humans is encoded by the RELB gene.

<span class="mw-page-title-main">REL</span> Protein-coding gene in the species Homo sapiens

The proto-oncogene c-Rel is a protein that in humans is encoded by the REL gene. The c-Rel protein is a member of the NF-κB family of transcription factors and contains a Rel homology domain (RHD) at its N-terminus and two C-terminal transactivation domains. c-Rel is a myeloid checkpoint protein that can be targeted for treating cancer. c-Rel has an important role in B-cell survival and proliferation. The REL gene is amplified or mutated in several human B-cell lymphomas, including diffuse large B-cell lymphoma and Hodgkin's lymphoma.

<span class="mw-page-title-main">BCL3</span> Protein-coding gene in the species Homo sapiens

B-cell lymphoma 3-encoded protein is a protein that in humans is encoded by the BCL3 gene.

<span class="mw-page-title-main">TANK-binding kinase 1</span> Protein-coding gene in the species Homo sapiens

TBK1 is an enzyme with kinase activity. Specifically, it is a serine / threonine protein kinase. It is encoded by the TBK1 gene in humans. This kinase is mainly known for its role in innate immunity antiviral response. However, TBK1 also regulates cell proliferation, apoptosis, autophagy, and anti-tumor immunity. Insufficient regulation of TBK1 activity leads to autoimmune, neurodegenerative diseases or tumorigenesis.

<span class="mw-page-title-main">CARD11</span> Protein-coding gene in the species Homo sapiens

Caspase recruitment domain-containing protein 11 also known as CARD-containing MAGUK protein 1 is a protein in the CARD-CC protein family that in humans is encoded by the CARD11 gene. CARD 11 is a membrane associated protein that is found in various human tissues, including the thymus, spleen, liver, and peripheral blood leukocytes. Similarly, CARD 11 is also found in abundance in various lines of cancer cells.

<span class="mw-page-title-main">NFKBIE</span> Protein-coding gene in the species Homo sapiens

Nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, epsilon, also known as NFKBIE, is a protein which in humans is encoded by the NFKBIE gene.

<span class="mw-page-title-main">MALT1</span> Protein-coding gene in the species Homo sapiens

Mucosa-associated lymphoid tissue lymphoma translocation protein 1 is a protein that in humans is encoded by the MALT1 gene. It's the human paracaspase.

<span class="mw-page-title-main">Toll-like receptor 11</span>

Toll-like receptor 11 (TLR11) is a protein that in mice and rats is encoded by the gene TLR11, whereas in humans it is represented by a pseudogene. TLR11 belongs to the toll-like receptor (TLR) family and the interleukin-1 receptor/toll-like receptor superfamily. In mice, TLR11 has been shown to recognise (bacterial) flagellin and (eukaryotic) profilin present on certain microbes, it helps propagate a host immune response. TLR11 plays a fundamental role in both the innate and adaptive immune responses, through the activation of Tumor necrosis factor-alpha, the Interleukin 12 (IL-12) response, and Interferon-gamma (IFN-gamma) secretion. TLR11 mounts an immune response to multiple microbes, including Toxoplasma gondii, Salmonella species, and uropathogenic E. coli, and likely many other species due to the highly conserved nature of flagellin and profilin.

Patrick Baeuerle is a German-based molecular biologist, immunologist, professor and a biopharmaceutical entrepreneur. Baeuerle is known for his work on tyrosine sulfation of proteins, transcription factor NF-kappaB, and the development of bispecific T-cell engaging antibodies for therapy of cancer.

<span class="mw-page-title-main">NFKBID</span> Protein-coding gene in the species Homo sapiens

Nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, delta also known as IκBNS is a protein in humans that is encoded by the NFKBID gene.

Soumen Basak is an Indian immunologist and virologist at the National Institute of Immunology (NII). A former fellow of the Wellcome Trust DBT India Alliance, he is known for his studies on the NF-kappaB signaling system.

References