Krishanu Bhowmick

Plasmodium falciparum acetyltransferase GCN5 acts as a dual regulator of essential glycolytic enzyme phosphoglycerate mutase

Ankita Tehlan, Poonam Nagar, Krishanu Bhowmick, Amarjeet Kumar et autres

Lysine acetylation is emerging as a key player in cellular regulation across species by controlling the fate of metabolic proteins as well as modulating gene expression via histone modification. Phosphoglycerate mutase, a conserved enzyme of the sole energy-yielding pathway of glycolysis in …

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264: METABOLIC MARKERS IN HCC PROGRESSION

Bino Mathew, Kazufumi Ohshiro, Krishanu Bhowmick, Xiyan Xiang et autres

Sa1211: CELLULAR INTERACTIONS BETWEEN SIRT6 AND BII-SPECTRIN-D1089Y MUTANT IN HEPATOCELLULAR CANCER

Kazufumi Ohshiro, Xiyan Xiang, Xiaochun Yang, Krishanu Bhowmick et autres

180: AMMONIA-MEDIATED DISRUPTION OF TGF-B SIGNALING IN EARLY-ONSET COLORECTAL CANCER

Krishanu Bhowmick, Puja Ghosh, Xiyan Xiang, Xiaochun Yang et autres

Microbial metabolite ammonia disrupts TGF-β signaling to promote colon cancer

Krishanu Bhowmick, Xiaochun Yang, Taj Mohammad, Xiyan Xiang et autres

Colorectal cancer (CRC) is rising alarmingly in younger populations, potentially arising from factors, such as obesity, proinflammatory gut microbiome, and the accumulation of toxic metabolites. However, how metabolites such as ammonia impact key signaling pathways to promote CRC remains unclear. Our study …

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Recent advances in targeting obesity, with a focus on TGF-β signaling and vagus nerve innervation

Sahara John, Krishanu Bhowmick, Andrew Park, Hai Huang et autres

Over a third of the global population is affected by obesity, fatty liver disease (Metabolic Dysfunction-Associated Steatotic Liver Disease, MASLD), and its severe form, MASH (Metabolic Dysfunction-Associated Steatohepatitis), which can ultimately progress to hepatocellular carcinoma (HCC). Recent advancements include therapeutics such as …

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Abstract 6533: Microbial metabolite ammonia disrupts CEACAM1 TGF-β signaling to drive colon cancer progression

Krishanu Bhowmick, Puja Ghosh, Xiyan Xiang, Xiaochun Yang et autres

Abstract Background: Colorectal cancer (CRC) is rising alarmingly in younger populations, potentially arising from additional risk factors such as obesity, pro-inflammatory microbiomes and accumulation of toxic metabolites. However, how metabolites such as ammonia impact key signaling pathways to promote CRC remains unclear. …

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Abstract 5181: SPTBN1D1089Y/+ aggravates liver carcinogenesis via activating SIRT6 and TGF-beta signaling

Kazufumi Ohshiro, Xiyan Xiang, Xiaochun Yang, Krishanu Bhowmick et autres

Abstract Background: Obese-driven liver cancer (HCC) is alarmingly rising in the US. Yet, key signaling mechanisms underlying this obesity-driven HCC remain unclear. SIRT6 is a NAD+-dependent deacetylase that limits the activity of the lipogenic transcription factors SREBP1/2 and TGF-β signaling. Reduced SIRT6 …

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Abstract 6671: Metabolic predictors in hepatocellular cancer

Bino Mathew, Kazufumi Ohshiro, Krishanu Bhowmick, Xiyan Xiang et autres

Background: Obesity and Metabolic dysfunction-associated steatotic liver disease (MASLD) affect nearly a third of the world's population. 20% of MASLD patients progress to Metabolic dysfunction-associated steatohepatitis (MASH). Hepatocellular Cancer (HCC) arises in 4-11% of MASH patients. Recently, we discovered obesity-driven cancers in …

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Author response for "Plasmodium falciparum acetyltransferase GCN5 acts as a dual regulator of essential glycolytic enzyme phosphoglycerate mutase"

Ankita Tehlan, Poonam Nagar, Krishanu Bhowmick, Amarjeet Kumar et autres

Author response for "Plasmodium falciparum acetyltransferase GCN5 acts as a dual regulator of essential glycolytic enzyme phosphoglycerate mutase"

Ankita Tehlan, Poonam Nagar, Krishanu Bhowmick, Amarjeet Kumar et autres

Aldehydes alter TGF-β signaling and induce obesity and cancer

Xiaochun Yang, Krishanu Bhowmick, Shuyun Rao, Xiyan Xiang et autres

mice. This study identifies SPTBN1 as a critical regulator of the functional phenotype of toxic aldehyde-induced MASH and a potential therapeutic target.

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