Sona Kang

ORCID: 0000-0002-9831-677X
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About
Contact & Profiles
Research Areas
  • Adipose Tissue and Metabolism
  • Adipokines, Inflammation, and Metabolic Diseases
  • Epigenetics and DNA Methylation
  • Lipid metabolism and biosynthesis
  • Metabolism, Diabetes, and Cancer
  • Cancer-related gene regulation
  • Wnt/β-catenin signaling in development and cancer
  • Diet and metabolism studies
  • Muscle metabolism and nutrition
  • IL-33, ST2, and ILC Pathways
  • Mitochondrial Function and Pathology
  • Vitamin D Research Studies
  • Research in Cotton Cultivation
  • Exercise and Physiological Responses
  • Genetic Syndromes and Imprinting
  • Immune cells in cancer
  • RNA modifications and cancer
  • Pancreatic function and diabetes
  • Hormonal Regulation and Hypertension
  • Immune Cell Function and Interaction
  • Peroxisome Proliferator-Activated Receptors
  • Signaling Pathways in Disease
  • Histone Deacetylase Inhibitors Research
  • Medicinal Plants and Neuroprotection
  • Kruppel-like factors research

University of California, Berkeley
2016-2025

Beth Israel Deaconess Medical Center
2010-2016

Harvard University
2012-2016

Union Hospital
2016

Brigham and Women's Hospital
2016

Huazhong University of Science and Technology
2016

University of Hong Kong
2016

Boston University
2016

Union Hospital
2016

University of Dubrovnik
2013

Mesenchymal precursor cells have the potential to differentiate into several cell types, including adipocytes and osteoblasts. Activation of Wnt/beta-catenin signaling shifts mesenchymal fate toward osteoblastogenesis at expense adipogenesis; however, molecular mechanisms by which Wnt alters not been fully investigated. Our prior work indicates that multipotent precursors express adipogenic osteoblastogenic transcription factors physiological levels ectopic expression Wnt10b in bipotential...

10.1074/jbc.m700030200 article EN cc-by Journal of Biological Chemistry 2007-03-11

Wnt is a family of secreted signaling proteins that regulate diverse developmental processes. Activation canonical by Wnt10b inhibits differentiation preadipocytes in vitro. To determine whether blocks adipogenesis vivo, we created transgenic mice which expressed from the FABP4 promoter. Expression adipose impairs development this tissue throughout body, with decline ∼50% total body fat and reduction ∼60% weight epididymal perirenal depots. FABP4-Wnt10b resist accumulation when fed high...

10.1074/jbc.m402937200 article EN cc-by Journal of Biological Chemistry 2004-06-15

The Wnt family of secreted signaling molecules has profound effects on diverse developmental processes, including the fate mesenchymal progenitors. While activation blocks adipogenesis, inhibition endogenous Wnt/beta-catenin by Wnt10b promotes spontaneous preadipocyte differentiation. Transgenic mice with expression from FABP4 promoter (FABP4-Wnt10b) have less adipose tissue when maintained a normal chow diet and are resistant to diet-induced obesity. Here we demonstrate that FABP4-Wnt10b...

10.2337/db06-1339 article EN Diabetes 2007-01-26

The chronic inflammatory state that accompanies obesity is a major contributor to insulin resistance and other dysfunctional adaptations in adipose tissue. Cellular secreted factors promote the milieu of obesity, but transcriptional pathways drive these processes are not well described. Although canonical transcription factor NF-κB considered be driver adipocyte inflammation, members interferon regulatory (IRF) family may also play role this process. Here, we determined IRF3 expression...

10.1172/jci86080 article EN Journal of Clinical Investigation 2016-07-10

We report that extended exposure to broad-spectrum terahertz radiation results in specific changes cellular functions are closely related DNA-directed gene transcription. Our chip survey of expression shows whereas 89% the protein coding genes mouse stem cells do not respond applied radiation, certain activated, while other repressed. RT-PCR experiments with selected probes corresponding transcripts three groups detail effect. The response was only but also irradiation conditions dependent....

10.1371/journal.pone.0015806 article EN cc-by PLoS ONE 2010-12-31

While there has been significant progress in determining the transcriptional cascade involved terminal adipocyte differentiation, less is known about early events leading to lineage commitment and cell fate choice. It recently discovered that zinc finger protein 423 (Zfp423) an actor adipose determination. Here, we show a close paralog of Zfp423, Zfp521, acts as key regulator differentiation vitro vivo. Zfp521 exerts its actions by binding B factor 1 (Ebf1), transcription required for...

10.1371/journal.pbio.1001433 article EN cc-by PLoS Biology 2012-11-27

The pathogenesis of insulin resistance involves dysregulated gene expression and function in multiple cell types, including endothelial cells (ECs). Post-transcriptional mechanisms such as microRNA-mediated regulation could affect action by modulating EC function. To determine whether microRNA-181b (miR-181b) affects the regulating white adipose tissue during obesity. MiR-181b was reduced ECs obese mice, rescue miR-181b improved glucose homeostasis sensitivity. Systemic intravenous delivery...

10.1161/circresaha.115.308166 article EN Circulation Research 2016-02-14

Interferon regulatory factors (IRFs) play functionally diverse roles in the transcriptional regulation of immune system. We have previously shown that several IRFs are regulators adipogenesis and IRF4 is a critical regulator adipocyte lipid handling. However, functional role adipose tissue macrophages (ATMs) remains unclear, despite high expression there. Here we show regulated primary ATMs high-fat diet-induced obese mice. Irf4(-/-) produce higher levels proinflammatory cytokines, including...

10.2337/db12-1327 article EN cc-by-nc-nd Diabetes 2013-07-09

Insulin resistance results from an intricate interaction between genetic make-up and environment, thus may be orchestrated by epigenetic mechanisms like DNA methylation. Here, we demonstrate that methyltransferase 3a (Dnmt3a) is both necessary sufficient to mediate insulin in cultured mouse human adipocytes. Furthermore, adipose-specific Dnmt3a knock-out mice are protected diet-induced glucose intolerance without accompanying changes adiposity. Unbiased gene profiling studies revealed Fgf21...

10.7554/elife.30766 article EN cc-by eLife 2017-11-01

Activation of canonical Wnt signaling inhibits brown adipogenesis cultured cells by impeding induction PPARγ and C/EBPα. Although enforced expression these adipogenic transcription factors restores lipid accumulation FABP4 in Wnt-expressing cells, additional PGC-1α is required for activation uncoupling protein 1 (UCP1). Wnt10b blocks adipose tissue development UCP1 when expressed from the fatty acid binding 4 promoter, even mice are administered a β3-agonist. In differentiated adipocytes,...

10.1128/mcb.25.4.1272-1282.2005 article EN Molecular and Cellular Biology 2005-02-01

Abstract It has been suggested that beige fat thermogenesis is tightly controlled by epigenetic regulators sense environmental cues such as temperature. Here, we report subcutaneous adipose expression of the DNA demethylase TET1 suppressed cold and other stimulators adipocyte thermogenesis. acts an autonomous repressor key thermogenic genes, including Ucp1 Ppargc1a , in adipocytes. Adipose-selective Tet1 knockout mice generated using Fabp4-Cre improves tolerance increases energy expenditure...

10.1038/s41467-020-18054-y article EN cc-by Nature Communications 2020-08-27

<p dir="ltr">Adipocyte hypertrophy significantly contributes to insulin resistance and metabolic dysfunction. Our previous research established JMJD8 as a mediator of resistance, noting its role in promoting adipocyte within an autonomous context. Nevertheless, the precise mechanisms underlying this phenomenon remained elusive. In study, we employed proteomics approach identify Perilipin 2 (PLIN2), lipid-associated protein, binding partner JMJD8. investigations unveiled robust...

10.2337/figshare.28152380.v1 preprint EN cc-by-nc-sa 2025-01-09

Adipocyte hypertrophy significantly contributes to insulin resistance and metabolic dysfunction. Our previous research established JMJD8 as a mediator of resistance, noting its role in promoting adipocyte within an autonomous context. Nevertheless, the precise mechanisms underlying this phenomenon remained elusive. In study, we employed proteomics approach identify Perilipin 2 (PLIN2), lipid-associated protein, binding partner JMJD8. investigations unveiled robust interaction between PLIN2,...

10.2337/db23-0883 article EN Diabetes 2025-01-09

<p dir="ltr">Adipocyte hypertrophy significantly contributes to insulin resistance and metabolic dysfunction. Our previous research established JMJD8 as a mediator of resistance, noting its role in promoting adipocyte within an autonomous context. Nevertheless, the precise mechanisms underlying this phenomenon remained elusive. In study, we employed proteomics approach identify Perilipin 2 (PLIN2), lipid-associated protein, binding partner JMJD8. investigations unveiled robust...

10.2337/figshare.28152380 preprint EN cc-by-nc-sa 2025-01-09

We previously identified the small molecule harmine as a regulator of peroxisome proliferator activated-receptor gamma (PPARgamma) and adipocyte differentiation. In an effort to identify signaling pathways mediating harmine's effects, we performed transcriptional profiling 3T3-F442A preadipocytes. Inhibitor DNA biding 2 (Id2) was gene rapidly induced by but not PPARgamma agonists. Id2 is also in 3T3-L1 preadipocytes treated with dexamethasone, 3-isobutyl-1-methylxanthine, insulin, suggesting...

10.1210/me.2007-0454 article EN Molecular Endocrinology 2008-06-19
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