Author

M. G. Kolonin

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Physiology· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:cell type annotation· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:differential expression· 1 Assay:DNA methylation· 1

Frequent Co-Authors

A. C. Daquinag· 1 shared A. G. Guzman· 1 shared A. R. Cox· 1 shared A. Tovy· 1 shared C. Rosas· 1 shared C.-W. Chen· 1 shared D. Park· 1 shared E. De Frutos Gonzalez· 1 shared

Activity by Year

2018-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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1 shared paperCell Biology

A. C. Daquinag

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3 papers

Recent·Most cited

Mesenchymal-specific Alms1 knockout in mice recapitulates key metabolic features of Alström Syndrome

E. J. McKay, I. Luijten, X. Weng, P. B. Martinez de Morentin, E. De Frutos Gonzalez, Z. Gao, M. G. Kolonin, L. K. Heisler, R. K. Semple

This study shows that deleting Alms1 in mesenchymal cells in mice causes metabolic issues similar to Alström Syndrome, including insulin resistance and fatty liver.

bioRxiv · Oct 12, 2023Physiology

Constitutive loss of DNMT3A causes morbid obesity through misregulation of adipogenesis

A. Tovy, J. M. Reyes, L. Zhang, Y.-H. Huang, C. Rosas, A. C. Daquinag, A. G. Guzman, R. Ramabadran, C.-W. Chen, T. Gu, S. Gupta, L. Ortinau, D. Park, A. R. Cox, R. E. Rau, , M. A. Goodell

This study shows that loss of DNMT3A causes obesity by disrupting adipogenesis and triggering inflammation in adipose tissue.

eLife · May 30, 2022Peer-reviewedCell Biology

Transient Overexpression of VEGF-A in Adipose Tissue Promotes Energy Expenditure via Activation of the Sympathetic Nervous System

Y. Zhao, X. Li, L. Yang, K. Eckel-Mahan, Q. Tong, X. Gu, M. G. Kolonin, K. Sun

This study shows that transient VEGF-A overexpression in adipose tissue activates the sympathetic nervous system, enhancing lipolysis, browning, and energy expenditure.

bioRxiv · May 16, 2018Physiology