Age, Biography and Wiki
Thirumala-Devi Kanneganti was born on 1972, is a Woman immunologist. Discover Thirumala-Devi Kanneganti's Biography, Age, Height, Physical Stats, Dating/Affairs, Family and career updates. Learn How rich is She in this year and how She spends money? Also learn how She earned most of networth at the age of 51 years old?
| Popular As | N/A |
| Occupation | N/A |
| Age | 51 years old |
| Zodiac Sign | N/A |
| Born | , 1972 |
| Birthday | |
| Birthplace | Kothagudem, India |
| Nationality |
We recommend you to check the complete list of Famous People born on . She is a member of famous with the age 51 years old group.
Thirumala-Devi Kanneganti Height, Weight & Measurements
At 51 years old, Thirumala-Devi Kanneganti height not available right now. We will update Thirumala-Devi Kanneganti's Height, weight, Body Measurements, Eye Color, Hair Color, Shoe & Dress size soon as possible.
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| Height | Not Available |
| Weight | Not Available |
| Body Measurements | Not Available |
| Eye Color | Not Available |
| Hair Color | Not Available |
Dating & Relationship status
She is currently single. She is not dating anyone. We don't have much information about She's past relationship and any previous engaged. According to our Database, She has no children.
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| Parents | Not Available |
| Husband | Not Available |
| Sibling | Not Available |
| Children | Not Available |
Thirumala-Devi Kanneganti Net Worth
Her net worth has been growing significantly in 2022-2023. So, how much is Thirumala-Devi Kanneganti worth at the age of 51 years old? Thirumala-Devi Kanneganti’s income source is mostly from being a successful . She is from . We have estimated Thirumala-Devi Kanneganti's net worth , money, salary, income, and assets.
| Net Worth in 2023 | $1 Million - $5 Million |
| Salary in 2023 | Under Review |
| Net Worth in 2022 | Pending |
| Salary in 2022 | Under Review |
| House | Not Available |
| Cars | Not Available |
| Source of Income |
Thirumala-Devi Kanneganti Social Network
Timeline
Kanneganti's lab has also been working on the upstream regulatory mechanisms of NLRP3 and identified caspase-8 and FADD as expression and activation regulators of both the canonical and non-canonical NLRP3 inflammasome/pyroptosis. This study demonstrated that the NLRP3 inflammasome/pyroptotic pathway is closely connected to the caspase-8–mediated programmed cell death pathway. This finding went against the dogma that existed at that time that caspase-8 and FADD were involved only in the apoptotic pathway. Following up on her original discovery that NLRP3 senses viral RNAs, her lab has discovered Z-DNA binding protein 1 (ZBP1)/DAI as an innate sensor of influenza virus upstream of the NLRP3 inflammasome/pyroptosis and also showed ZBP1 is a key regulator of apoptosis and necroptosis, establishing it as a master regulator of these cell death pathways. Her lab also established that transforming growth factor beta-activated kinase 1 (TAK1) can act as a master regulator that maintains cellular homeostasis by negatively regulating the NLRP3 inflammasome and pyroptosis, apoptosis, and necroptosis. Overall, these studies identified caspase-8, ZBP1, and TAK1 as master molecular switches of inflammasome activation/pyroptosis, apoptosis, and necroptosis and pioneered the emergence of the PANoptosis (Pyroptosis, Apoptosis, Necroptosis) concept, which describes the integration of the pyroptosis, apoptosis, and necroptosis pathways into a unified mechanism of cell death executed through a single multiprotein complex, the PANoptosome. Kanneganti's research group recently further elucidated the molecular mechanism of PANoptosis and showed that the enigmatic caspase-6 is critical for ZBP1-mediated NLRP3 inflammasome activation, PANoptosis, innate immune responses, and host defense against IAV.
Kanneganti began her career in research with her time as a PhD student studying plant pathogens and fungal toxins. She then went on to do postdoctoral fellowships at the University of Wisconsin and the Ohio State University studying fungal genetics and plant innate immunity. She then transitioned to study mammalian innate immunity at the University of Michigan. She joined St. Jude Children's Research Hospital as an Assistant Member in the Immunology Department in 2007, where she has focused on studying inflammasomes. She was promoted to a full Member in 2013. She became Vice Chair of the Immunology Department in 2016 and was endowed with the Rose Marie Thomas Endowed Chair in 2017.
Kanneganti has made fundamental contributions to inflammasome biology. Her studies along with those from other groups published in 2006 provided the first genetic evidence for the role of NLRP3 in the formation of the inflammasome, caspase-1 activation, and IL-1β/IL-18 maturation. These initial studies showed that microbial components, ATP, and MSU crystals activate the NLRP3 inflammasome. Dr. Kanneganti discovered that Influenza A virus, Candida, and Aspergillus specifically activate the NLRP3 inflammasome and elucidated the physiological role of the NLRP3 inflammasome in host defense. In addition to these studies on the role of the NLRP3 inflammasome in infectious diseases, her lab also established the importance of the NLRP3 inflammasome in intestinal inflammation, neuroinflammation, cancer, and obesity.
In addition to the original discoveries published in 2006 on the NLRP3 inflammasome, Kanneganti's work has also contributed to the identification of bacterial flagellin as a ligand that activates the NLRC4 inflammasome. Her lab also identified interferon regulatory factor 8 (IRF8) as a specific upstream regulator of NLRC4 and discovered the role of the IRF1-GBP-IRGB10 pathway in liberating intracellular bacterial ligands that are eventually sensed by the AIM2 and NLRP3 inflammasomes. These studies linked IRFs to the NLRC4, NLRP3, and AIM2 inflammasomes. Furthermore, her lab also identified a critical role for AIM2 in stem cell proliferation and cancer. In addition, her work has delineated an important role for NLRC3 in safe-guarding the intestine from overt proliferation and cancer via mTOR regulation. Dr. Kanneganti's lab has also discovered an essential role for the pyrin (MEFV) inflammasome in the maintenance of intestinal barrier integrity to prevent colitis and colitis-associated cancer. Her studies also showed the physiological significance of caspase-1 and IL-1β downstream of pyrin inflammasome activation in mediating familial Mediterranean fever (FMF) and also identified the role of the TNF/TNFR axis in promoting pyrin inflammasome activation.
Thirumala-Devi Kanneganti (born 1972) is an immunologist and is the Rose Marie Thomas Endowed Chair, Vice Chair of the Department of Immunology, and Member at St. Jude Children's Research Hospital. Her research interests include innate immunity with a primary focus on the role of NLR proteins and inflammasomes in health and disease.
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