"Recently, NIH has funded a center for autophagy research named the Autophagy, Inflammation, and Metabolism (AIM) Center of Biomedical Research Excellence, located at the University of New Mexico Health Science Center (UNM HSC), with aspirations to promote autophagy research locally, nationally, and internationally."
Check out the editorial published by Taylor & Francis Online.
AIM center researchers, Drs. Meilian Liu and Xuexian Yang et all; have just published their findings in Nature - Scientific Reports on the "... previously unappreciated insight that obesity-associated hyperleptinemia contributes to enhanced pro-allergic lymphocyte responses through induction of XBP1s, leading to exacerbation of allergic asthma."
RAC3 is a member of the p160 family of steroid receptor coactivators and it is highly expressed in several human cancers, contributing to enhanced cell proliferation and cellular transformation...
At high cell density or when plated on soft matrix, YAP/TAZ are redistributed from the nucleus to the cytosol, becoming transcriptionally inactive. Here the authors show that at high cell density, autophagosome formation is impaired due to reduced YAP/TAZ-dependent transcription of actomyosin gene
During autophagy, phagophores elongate to form double-membrane vesicles but the mechanism behind their closure is unknown. Here, the authors develop an autophagy assay and find a role for the endosomal sorting complexes required for transport component CHMP2A as a phagophore closure regulator.
Many Amyotrophic Lateral Sclerosis (ALS)-linked mutations cause accumulation of stress granules, and most ALS cases are caused by repeat expansions in C9ORF72. Here the authors show that C9ORF72 and the autophagy receptor p62 interact to associate with proteins symmetrically dimethylated on arginines such as FUS, to eliminate stress granules by autophagy.