Klotho Ameliorates Chemically Induced Endoplasmic Reticulum (ER) Stress Signaling | Zendy

Srijita Banerjee | Zendy; Yanhua Zhao | Zendy; Partha S. Sarkar | Zendy; Kevin P. Rosenblatt | Zendy; Ronald G. Tilton | Zendy; Sanjeev Choudhary | Zendy

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Klotho Ameliorates Chemically Induced Endoplasmic Reticulum (ER) Stress Signaling

Author(s) -

Srijita Banerjee,

Yanhua Zhao,

Partha S. Sarkar,

Kevin P. Rosenblatt,

Ronald G. Tilton,

Sanjeev Choudhary

Publication year - 2013

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000350085

Subject(s) - thapsigargin , unfolded protein response , tunicamycin , endoplasmic reticulum , endocrinology , klotho , chop , microbiology and biotechnology , apoptosis , medicine , chemistry , a549 cell , cancer research , biology , kidney , biochemistry

Both endoplasmic reticulum (ER) stress, a fundamental cell response associated with stress-initiated unfolded protein response (UPR), and loss of Klotho, an anti-aging hormone linked to NF-κB-induced inflammation, occur in chronic metabolic diseases such as obesity and type 2 diabetes. We investigated if the loss of Klotho is causally linked to increased ER stress.

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