Редактирование: BAG3

BAG family molecular chaperone regulator 3 (BAG-3) (Bcl-2-associated athanogene 3) (Bcl-2-binding protein Bis) (Docking protein CAIR-1) [BIS]

==Publications==

{{medline-entry
|title=Nrf2 mediates the expression of [[BAG3]] and autophagy cargo adaptor proteins and tau clearance in an age-dependent manner.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29304346
|abstract=During aging, decreased efficiency of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activation and autophagic processes in the brain may be a contributing factor in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease. Therefore, we analyzed the expression of Bcl-2-associated athanogene 3, a cochaperone that mediates autophagy, and the autophagy adaptors [[NBR1]], NDP52, and sequestosome 1/p62 in the brains of 4-, 8-, and 12-month-old wild-type and Nrf2 knockout (-/-) mice. We also analyzed the levels of total tau and phospho-tau species. There were minimal differences in the expression of autophagy-related genes or tau species in 4-month-old animals; however, by 12 months, all of these autophagy-associated genes were expressed at significantly lower levels in the Nrf2 (-/-) mice. The decreases in the autophagy-associated genes were accompanied by significantly elevated levels of phospho-tau species in the 12-month-old Nrf2 (-/-) brains. These findings indicate that Nrf2 regulation of autophagy-related genes likely plays a greater role in mediating the clearance of tau as an organism ages.
|mesh-terms=* Adaptor Proteins, Signal Transducing
* Aging
* Alzheimer Disease
* Animals
* Apoptosis Regulatory Proteins
* Autophagy
* Autophagy-Related Proteins
* Brain
* Gene Expression
* Mice, Inbred C57BL
* Mice, Knockout
* NF-E2-Related Factor 2
* Neurodegenerative Diseases
* tau Proteins
|keywords=* Autophagy adaptors
* BAG3
* Nrf2
* Tau
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5801049
}}
{{medline-entry
|title=Age-related obesity and type 2 diabetes dysregulate neuronal associated genes and proteins in humans.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26337083
|abstract=Despite numerous developed drugs based on glucose metabolism interventions for treatment of age-related diseases such as diabetes neuropathies (DNs), DNs are still increasing in patients with type 1 or type 2 diabetes (T1D, T2D). We aimed to identify novel candidates in adipose tissue (AT) and pancreas with T2D for targeting to develop new drugs for DNs therapy. AT-T2D displayed 15 (e.g. [[SYT4]] up-regulated and [[VGF]] down-regulated) and pancreas-T2D showed 10 (e.g. [[BAG3]] up-regulated, [[VAV3]] and [[APOA1]] down-regulated) highly differentially expressed genes with neuronal functions as compared to control tissues. ELISA was blindly performed to measure proteins of 5 most differentially expressed genes in 41 human subjects. [[SYT4]] protein was upregulated, [[VAV3]] and [[APOA1]] were down-regulated, and [[BAG3]] remained unchanged in 1- Obese and 2- Obese-T2D without insulin, [[VGF]] protein was higher in these two groups as well as in group 3- Obese-T2D receiving insulin than 4-lean subjects. Interaction networks analysis of these 5 genes showed several metabolic pathways (e.g. lipid metabolism and insulin signaling). Pancreas is a novel site for [[APOA1]] synthesis. [[VGF]] is synthesized in AT and could be considered as good diagnostic, and even prognostic, marker for age-induced diseases obesity and T2D. This study provides new targets for rational drugs development for the therapy of age-related DNs. 
|mesh-terms=* Adaptor Proteins, Signal Transducing
* Adipose Tissue
* Adult
* Aged
* Analysis of Variance
* Apolipoprotein A-I
* Apoptosis Regulatory Proteins
* Diabetes Mellitus, Type 2
* Enzyme-Linked Immunosorbent Assay
* Female
* Gene Expression Profiling
* Gene Expression Regulation
* Humans
* Hypoglycemic Agents
* Insulin
* Male
* Middle Aged
* Nerve Growth Factors
* Neurons
* Obesity
* Pancreas
* Proto-Oncogene Proteins c-vav
* Reverse Transcriptase Polymerase Chain Reaction
* Synaptotagmins
|keywords=* age-related diabetes neuropathy
* aging
* diabetes
* obesity
* pancreas
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4745765
}}