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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=BAG3</id>
	<title>BAG3 - История изменений</title>
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	<updated>2026-06-09T08:17:19Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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		<id>https://transhumanist.ru/index.php?title=BAG3&amp;diff=4043&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «BAG family molecular chaperone regulator 3 (BAG-3) (Bcl-2-associated athanogene 3) (Bcl-2-binding protein Bis) (Docking protein CAIR-1) [BIS]  ==Publications==  {...»</title>
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		<updated>2021-04-29T18:57:49Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «BAG family molecular chaperone regulator 3 (BAG-3) (Bcl-2-associated athanogene 3) (Bcl-2-binding protein Bis) (Docking protein CAIR-1) [BIS]  ==Publications==  {...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;BAG family molecular chaperone regulator 3 (BAG-3) (Bcl-2-associated athanogene 3) (Bcl-2-binding protein Bis) (Docking protein CAIR-1) [BIS]&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=Nrf2 mediates the expression of [[BAG3]] and autophagy cargo adaptor proteins and tau clearance in an age-dependent manner.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29304346&lt;br /&gt;
|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&amp;#039;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.&lt;br /&gt;
|mesh-terms=* Adaptor Proteins, Signal Transducing&lt;br /&gt;
* Aging&lt;br /&gt;
* Alzheimer Disease&lt;br /&gt;
* Animals&lt;br /&gt;
* Apoptosis Regulatory Proteins&lt;br /&gt;
* Autophagy&lt;br /&gt;
* Autophagy-Related Proteins&lt;br /&gt;
* Brain&lt;br /&gt;
* Gene Expression&lt;br /&gt;
* Mice, Inbred C57BL&lt;br /&gt;
* Mice, Knockout&lt;br /&gt;
* NF-E2-Related Factor 2&lt;br /&gt;
* Neurodegenerative Diseases&lt;br /&gt;
* tau Proteins&lt;br /&gt;
|keywords=* Autophagy adaptors&lt;br /&gt;
* BAG3&lt;br /&gt;
* Nrf2&lt;br /&gt;
* Tau&lt;br /&gt;
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5801049&lt;br /&gt;
}}&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=Age-related obesity and type 2 diabetes dysregulate neuronal associated genes and proteins in humans.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26337083&lt;br /&gt;
|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. &lt;br /&gt;
|mesh-terms=* Adaptor Proteins, Signal Transducing&lt;br /&gt;
* Adipose Tissue&lt;br /&gt;
* Adult&lt;br /&gt;
* Aged&lt;br /&gt;
* Analysis of Variance&lt;br /&gt;
* Apolipoprotein A-I&lt;br /&gt;
* Apoptosis Regulatory Proteins&lt;br /&gt;
* Diabetes Mellitus, Type 2&lt;br /&gt;
* Enzyme-Linked Immunosorbent Assay&lt;br /&gt;
* Female&lt;br /&gt;
* Gene Expression Profiling&lt;br /&gt;
* Gene Expression Regulation&lt;br /&gt;
* Humans&lt;br /&gt;
* Hypoglycemic Agents&lt;br /&gt;
* Insulin&lt;br /&gt;
* Male&lt;br /&gt;
* Middle Aged&lt;br /&gt;
* Nerve Growth Factors&lt;br /&gt;
* Neurons&lt;br /&gt;
* Obesity&lt;br /&gt;
* Pancreas&lt;br /&gt;
* Proto-Oncogene Proteins c-vav&lt;br /&gt;
* Reverse Transcriptase Polymerase Chain Reaction&lt;br /&gt;
* Synaptotagmins&lt;br /&gt;
|keywords=* age-related diabetes neuropathy&lt;br /&gt;
* aging&lt;br /&gt;
* diabetes&lt;br /&gt;
* obesity&lt;br /&gt;
* pancreas&lt;br /&gt;
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4745765&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
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