βA1-crystallin regulates glucose metabolism and mitochondrial function in mouse retinal astrocytes by modulating PTP1B activity

βA1-crystallin regulates glucose metabolism and mitochondrial function in mouse retinal astrocytes by modulating PTP1B activity

Ghosh et al. show that a lens protein βA1-crystallin inhibits PTP1B activity, regulating the metabolism of retinal astrocytes. They find that knockdown of βA1-crystallin exacerbates the streptozotocin-induced diabetic retinopathy-like phenotype in mice, suggesting the possibility that the interactio...

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Autores principales: Sayan Ghosh, Haitao Liu, Meysam Yazdankhah, Nadezda Stepicheva, Peng Shang, Tanuja Vaidya, Stacey Hose, Urvi Gupta, Michael Joseph Calderon, Ming-Wen Hu, Archana Padmanabhan Nair, Joseph Weiss, Christopher S. Fitting, Imran A. Bhutto, Santosh Gopi Krishna Gadde, Naveen Kumar Naik, Chaitra Jaydev, Gerard A. Lutty, James T. Handa, Ashwath Jayagopal, Jiang Qian, José-Alain Sahel, Dhivyaa Rajasundaram, Yuri Sergeev, J. Samuel Zigler, Swaminathan Sethu, Simon Watkins, Arkasubhra Ghosh, Debasish Sinha
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
Materias:
Biology (General)
QH301-705.5
Acceso en línea:https://doaj.org/article/73f2d2042a5b442cb0991f9ae494dfe7
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Sumario:Ghosh et al. show that a lens protein βA1-crystallin inhibits PTP1B activity, regulating the metabolism of retinal astrocytes. They find that knockdown of βA1-crystallin exacerbates the streptozotocin-induced diabetic retinopathy-like phenotype in mice, suggesting the possibility that the interaction between βA1-PTP1B may be targeted for diabetic retinopathy.

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