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Deletion of Bmal1 in Intestinal Epithelium Protects against Colonic Inflammation by Suppressing the Apoptosis Pathway I

ABSTRACT: Deletion of Bmal1 in Intestinal Epithelium Protects against Colonic Inflammation by Suppressing the Apoptosis Pathway I

PROVIDER: PRJNA1065494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27585021_1.fastq.gz	Fastqsanger.gz
	SRR27585021_2.fastq.gz	Fastqsanger.gz
	SRR27585022_1.fastq.gz	Fastqsanger.gz
	SRR27585022_2.fastq.gz	Fastqsanger.gz
	SRR27585023_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Deletion of Bmal1 in Intestinal Epithelium Protects against Colonic Inflammation by Suppressing the Apoptosis Pathway

Project description:Deletion of Bmal1 in Intestinal Epithelium Protects against Colonic Inflammation by Suppressing the Apoptosis Pathway

| PRJNA1130403 | ENA

Deletion of Bmal1 in Intestinal Epithelium Protects against Colonic Inflammation by Suppressing the Apoptosis Pathway

Project description:Deletion of Bmal1 in Intestinal Epithelium Protects against Colonic Inflammation by Suppressing the Apoptosis Pathway

| PRJNA1130917 | ENA

Deletion of Bmal1 in Intestinal Epithelium Protects against Colonic Inflammation by Suppressing the Apoptosis Pathway

Project description:The circadian clock has been shown to regulate inflammatory bowel disease (IBD), but the underlying mechanisms remain unclear. Here, we observed that the mice in the active phase of the circadian clock were more tolerant to dextrose sodium sulfate (DSS)-induced colitis, compared to those in the resting phase. Furthermore, we found that the circadian gene Bmal1 displayed a dynamic expression pattern in mouse colonic epithelium during the circadian clock, with a high level in the resting phase and a low in the active phase. Ablation of Bmal1 in the intestinal epithelium reduced inflammatory symptoms in the colon of the DSS-treated mice. The mice with Bmal1 deletion exhibited no obvious disruption on intestinal homeostasis, rather were more resistant to DSS-induced inflammation, with less body weight change, fewer pathological symptoms, and greater epithelial integrity, compared to the control group. Mechanistically, BMAL1 promoted apoptosis by binding to the apoptosis-related genes, such as Bax, P53 and Bak1, and transcriptionally activating their expression. Collectively, our results reveal the Bmal1-centered circadian clock is involved in intestinal repair upon injure. Clinically, targeting Bmal1 function may be a promising approach to treat inflammation-related gastrointestinal tract diseases.

2025-04-28 | GSE271174 | GEO

Deletion of Bmal1 in Intestinal Epithelium Protects against Colonic Inflammation by Suppressing the Apoptosis Pathway I

2025-04-27 | GSE253421 | GEO

Deletion of Bmal1 in Intestinal Epithelium Protects against Colonic Inflammation by Suppressing the Apoptosis Pathway (CUT&Tag)

2025-04-29 | GSE254225 | GEO

Deletion of Bmal1 in Intestinal Epithelium Protects against Colonic Inflammation by Suppressing the Apoptosis Pathway (CUT&Tag)

Project description:Deletion of Bmal1 in Intestinal Epithelium Protects against Colonic Inflammation by Suppressing the Apoptosis Pathway (CUT&Tag)

| PRJNA1069044 | ENA

Deletion of Bmal1 in Intestinal Epithelium Protects against Colonic Inflammation by Suppressing the Apoptosis Pathway

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-04-27 | GSE271317 | GEO

Inhibition of TWEAK/Tnfrsf12a axis protects against acute liver failure by suppressing RIPK1-dependent apoptosis

Project description:Inhibition of TWEAK/Tnfrsf12a axis protects against acute liver failure by suppressing RIPK1-dependent apoptosis

| PRJNA851438 | ENA

TMT analysis of proteomic changes in the gastrocnemius skeletal muscles of WT and Bmal1-KO mice, and Bmal1-KO mice rescued with AAV-mediated muscle-specific expression of Bmal1.

Project description:TMT analysis of proteomic changes in the gastrocnemius skeletal muscles of WT and Bmal1-KO mice, and Bmal1-KO mice rescued with AAV-mediated muscle-specific expression of Bmal1.

2024-10-03 | PXD054406 | Pride

Proteomics analysis of regulation by Bmal1 and physiological time-restricted feeding

Project description:To define regulation of tissue proteomes by Bmal1, daily feeding rhythm, and the interaction, we employed Bmal1-stopFL mice, which do not express the main transcriptional activator of the molecular clock, Bmal1, except in cre recombinase-expressing cells1,2 (Figure 1A). Bmal1-stopFL mice lacking cre (Bmal1 knockout, KO) are analogous to Bmal1-null mice and display severely impaired behavioral and molecular rhythms1-3. Hepatocyte-specific Alfp-cre and skeletal muscle-specific Hsa-cre genes were introduced to generate a single line wherein both hepatocyte and skeletal muscle Bmal1 were reconstituted (Liver+Muscle-RE), i.e., rescued (Smith, Koronowski et al. 2023). This approach had the benefit of analyzing liver and muscle from the same mice but comes with the qualification that the abundance of some proteins may be influenced by Bmal1 function in the other tissue, or by a synergistic effect of Bmal1 in both tissues, rather than through rescue of local Bmal1 function alone. Proteomic anlaysis was performed in liver and skeletal muscle.

2024-01-26 | PXD040362 | Pride

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