Dataset Information

P16 ^{I NK 4a} Deletion Ameliorates Damage of Intestinal Epithelial Barrier and Microbial Dysbiosis in a Stress-Induced Premature Senescence Model of Bmi-1 Deficiency.

ABSTRACT: This study aimed to determine whether Bmi-1 deficiency leads to intestinal epithelial barrier destruction and microbiota dysfunction, which members of the microbial community alter barrier function with age, and whether p16 ^INK4a deletion could reverse the damage of intestinal epithelial barrier and microbial dysbiosis. Intestines from Bmi-1-deficient (Bmi-1^-/- ), Bmi-1 and p16 ^INK4a double-knockout (Bmi-1^-/-p16 ^INK4a-/- ), and wild-type mice were observed for aging and inflammation. Duolink Proximity Ligation Assay, immunoprecipitation, and construction of p16 ^INK4a overexpressed adenovirus and the overexpressed plasmids of full-length, muta

SUBMITTER: Zhou J

PROVIDER: S-EPMC8545785 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature

ACCESS DATA

Dataset Information

P16 ^{I NK 4a} Deletion Ameliorates Damage of Intestinal Epithelial Barrier and Microbial Dysbiosis in a Stress-Induced Premature Senescence Model of Bmi-1 Deficiency.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

P16 I NK 4a Deletion Ameliorates Damage of Intestinal Epithelial Barrier and Microbial Dysbiosis in a Stress-Induced Premature Senescence Model of Bmi-1 Deficiency.

OmicsDI is part of the ELIXIR infrastructure

Tweets

P16 ^{I NK 4a} Deletion Ameliorates Damage of Intestinal Epithelial Barrier and Microbial Dysbiosis in a Stress-Induced Premature Senescence Model of Bmi-1 Deficiency.