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Michael Karas

Researcher at National Institutes of Health

Publications -  17
Citations -  2022

Michael Karas is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Signal transduction & Insulin-like growth factor 1 receptor. The author has an hindex of 15, co-authored 17 publications receiving 1980 citations.

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Uncoupling Protein-3 Is a Mediator of Thermogenesis Regulated by Thyroid Hormone, β3-Adrenergic Agonists, and Leptin

TL;DR: UCP3 levels were greatly increased by treatment with the β3-adrenergic agonist, CL214613, suggesting another pathway for increasing thermogenesis and UCP3 mRNA levels were also regulated by dexamethasone, leptin, and starvation, albeit differently in muscle and brown adipose tissue.
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Insulin-like growth factor-I receptor signal transduction: at the interface between physiology and cell biology.

TL;DR: This review outlines some of the signalling pathways believed to be important in converting IGF-IR activation into changes in cell behavior and metabolism.
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Insulin-Like Growth Factor-I Affects Perinatal Lethality and Postnatal Development in a Gene Dosage-Dependent Manner: Manipulation Using the Cre/loxP System in Transgenic Mice

TL;DR: Cre-induced genomic recombination using the EIIa promoter occurs during development and creates distinct phenotypes compared with the conventional null mutation, which allows for postnatal survival and will enable one to begin to explore the role of the endocrine vs. paracrine effects of IGF-I.
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PTEN inhibits cell proliferation and induces apoptosis by downregulating cell surface IGF-IR expression in prostate cancer cells.

TL;DR: Results show that PTEN can regulate cell proliferation and apoptosis through inhibition of IGF-IR synthesis and have important implications for understanding the roles of PTEN and the IGF- IR in prostate cancer cell tumorigenesis.
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The potentiation of estrogen on insulin-like growth factor I action in MCF-7 human breast cancer cells includes cell cycle components.

TL;DR: It is suggested that in MCF-7 cells, estrogen potentiates the IGF-1 effect on IGF- 1R signaling as well as on the cell cycle components, and IGF-2 regulates the expression of p21 and p27 and their association with CDK2 differently.