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Literature summary for 2.3.1.B41 extracted from

  • Fan, Y.; Yang, Q.; Yang, Y.; Gao, Z.; Ma, Y.; Zhang, L.; Liang, W.; Ding, G.
    Sirt6 suppresses high glucose-induced mitochondrial dysfunction and apoptosis in podocytes through AMPK activation (2019), Int. J. Biol. Sci., 15, 701-713 .
    View publication on PubMedView publication on EuropePMC
Search for more literature for 2.3.1.B41

Localization

Localization Comment Organism GeneOntology No. Textmining
mitochondrion
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 Homo sapiens 5739
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mitochondrion
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 Mus musculus 5739
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Organism

Organism UniProt Comment Textmining
Homo sapiens Q8N6T7
-
-
Mus musculus P59941
-
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Mus musculus C57BL/6 P59941
-
-

Source Tissue

Source Tissue Comment Organism Textmining
cardiac muscle fiber
-
 Homo sapiens
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kidney
-
 Homo sapiens
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kidney
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 Mus musculus
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additional information Sirt6 expression and Sirt6-wild-type-1 colocalization is suppressed in the glomeruli of patients with diabetic nephropathy (DN) Homo sapiens
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additional information Sirt6 expression is reduced in the kidney of streptozotocin(STZ)-induced diabetic mice Mus musculus
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podocyte
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 Homo sapiens
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podocyte a dramatic reduction in Sirt6 is detected in the podocytes in diabetic mice relative to those in control mice Mus musculus
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skeletal muscle
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 Homo sapiens
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Synonyms

Synonyms Comment Organism
histone deacetylase
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 Homo sapiens
histone deacetylase
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 Mus musculus
SIRT6
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 Homo sapiens
SIRT6
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 Mus musculus
Sirtuin6
-
 Homo sapiens
Sirtuin6
-
 Mus musculus

Expression

Organism Comment Expression
Homo sapiens high-glucose causes Sirt6 and p-AMPK downregulation in podocytes. High-glucose conditions decrease Sirt6 expression levels significantly down
Mus musculus high-glucose conditions decrease Sirt6 expression levels significantly down

General Information

General Information Comment Organism
malfunction diabetic mice exhibit reduced Sirt6 expression and AMP kinase (AMPK) dephosphorylation accompanied by mitochondrial morphological abnormalities. Hyperglycemia-induced Sirt6 levels are decreased in vivo. Hyperglycemia promotes podocyte mitochondrial dysfunction in mice with diabetic nephropathy (DN) Mus musculus
malfunction in vitro, podocytes exposed to high-glucose present with mitochondrial morphological alterations and podocyte apoptosis accompanied by Sirt6 and p-AMPK downregulation. The mitochondrial defects induced by high-glucose are significantly alleviated by Sirt6 plasmid transfection. Sirt6 overexpression simultaneously alleviates high-glucose-induced podocyte apoptosis and oxidative stress, as well as increased AMPK phosphorylation. Increased levels of H3K9ac and H3K56ac induced by high-glucose are attenuated in podocytes transfected with Sirt6 plasmids. Cell apoptosis is significantly ameliorated after the transfection of the Sirt6 plasmid in high-glucose-stimulated podocytes Homo sapiens
physiological function histone deacetylase Sirtuin6 (Sirt6) has an essential role in the regulation of mitochondrial function in skeletal muscle and cardiomyocytes. Sirt6 also plays a specific role in mitochondrial homeostasis in podocytes. Analysis of the physiological function of Sirt6 in podocyte mitochondria and apoptosis under high-glucose conditions and mechanism, overview. Sirt6 suppresses high glucose-induced mitochondrial dysfunction and apoptosis in podocytes through AMPK activation Homo sapiens