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RNA-seq results in the liver of male hepatocyte-specific GAPDH knockout mice in fasting supplemented with or without serine

ABSTRACT: Our study represents the first detailed analysis of transcriptomes in liver of hepatocyte-specific GAPDH knockout mice to understand key pathways and regulatory genes, with biologic replicates, generated by RNA-seq technology

ORGANISM(S): Mus musculus

PROVIDER: GSE293050 | GEO | 2026/03/20

REPOSITORIES: GEO

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RNA-seq results in the liver of male hepatocyte-specific GAPDH knockout mice in fasting supplemented with or without serine

Project description:RNA-seq results in the liver of male hepatocyte-specific GAPDH knockout mice in fasting supplemented with or without serine

| PRJNA1242700 | ENA

Gene profile in H1299 cells treated with PTD-DRBD GAPDH siRNA or treated with Lipofection GAPDH siRNA

Project description:Whole genome microarrays were probed with total mRNA from PTD-DRBD GAPDH siRNA treated H1299 cells at 12 h and 24 h. Using a 1.6x fold increase/decrease filter of cellular mRNAs, we detected a dramatic reduction in the target GAPDH mRNA along with a limited number of both up and down regulated genes. The up regulated genes were reduced in numbers and to nearly background 1.6x levels at 24 h, while the down regulated genes increased slightly in numbers and maintained a similar magnitude at 24 h. In contrast, lipofection treated cells showed both a dramatic increase in both the total number of genes altered and the magnitude of the increase. In addition, the numbers of genes affected increased between 12 h and 24 h, suggesting that lipofection of siRNAs into cells results in a substantial alteration to the transcriptome and may thereby confound interpretation of experimental outcomes. Moreover, the GAPDH specific knockdown was significantly smaller than PTD-DRBD mediated knockdown.

2009-05-22 | GSE15723 | GEO

Gene profile in H1299 cells treated with PTD-DRBD GAPDH siRNA or treated with Lipofection GAPDH siRNA

2010-05-08 | E-GEOD-15723 | biostudies-arrayexpress

GAPDH Controls Transcript Stability, Protein Translation and Drives Proliferation in Acute Myeloid Leukemia [GAPDH_KD_RNAseq]

Project description:Dysregulation of RNA binding proteins (RBPs) is a hallmark in cancerous cells. In acute myeloid leukemia (AML) RBPs are key regulators of tumor proliferation. While classical RBPs have defined RNA binding domains, RNA recognition and function in AML by non-canonical RBPs (ncRBPs) remains unclear. Given the inherent complexity of targeting AML broadly, our goal was to uncover potential ncRBP candidates critical for AML survival using a CRISPR/Cas-based screening. We identified the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as a pro-proliferative factor in AML cells. Based on cross-linking and immunoprecipitation (CLIP) we are defining the global targetome detecting novel RNA targets mainly located within 5’UTR including GAPDH, RPL13a, PKM and ENO1. The knockdown of GAPDH unveiled genetic pathways related to ribosome biogenesis, translation initiation, and regulation. Moreover, we were able to demonstrate a stabilizing effect through the GAPDH binding to target transcripts including its own mRNA, unveiling GAPDH’s pivotal role in cancer. The present findings provide new insights on the pathophysiological role of GAPDH in AML.

2025-11-05 | GSE270169 | GEO

3-Hydroxypropionic acid converts inflammatory macrophage glycolysis into mitochondrial oxidation through GAPDH carboxyethylation

Project description:Macrophages dynamically reprogram their metabolic states in response to environmental stimuli, thereby exerting distinct immune functions. In our preliminary study, a gut microbiota-derived metabolite 3-hydroxypropionic acid (3-HPA) is increased in chronic inflammation and generates cysteine carboxyethylated neoantigens. However, the role of such metabolite-induced modification in regulating the function of macrophages remains obscure. Here, we show that 3-HPA alleviates inflammation in a mouse model of sepsis and inhibits the macrophage inflammatory response. Mechanistically, 3-HPA induces glyceraldehyde-3-phosphate dehydrogenase (GAPDH) carboxyethylation, which promotes GAPDH degradation via the ubiquitin-proteasome pathway, thereby suppressing its enzymatic activity and expression to inhibit glycolysis. Concomitantly, reduced GAPDH activity elevates the NAD+/NADH ratio, which enhances mitochondrial oxidation by upregulating arginine biosynthesis and the TCA cycle pathway. All above, our research reveals the mechanism by which GAPDH carboxyethylation mediates metabolic reprogramming and regulates inflammation during inflammatory macrophage activation.

2026-05-14 | GSE316690 | GEO

GAPDH Controls Transcript Stability, Protein Translation and Drives Proliferation in Acute Myeloid Leukemia [CLIP-seq]

2025-11-05 | GSE270168 | GEO

Role of hepatocyte NAMPT in fasting-induced liver gene expression

Project description:We tested they hypothesis that hepatocyte NAMPT mediates transcriptomic changes induced by fasting

2021-09-21 | GSE184395 | GEO

ChIP-Seq for nuclear GAPDH in ex-vivo cortical microglia from LPS treated mice

Project description:We report the genome wide map for the peaks of occupancy of nuclear GAPDH in cortical microglia from mice treated with LPS.

2023-07-31 | GSE155501 | GEO

HDX-MS data of trigger factor and GAPDH binding

Project description:We present HDX-MS data of the trigger factor:GAPDH complex to define the interaction sites for GAPDH on trigger factor and the structure of GAPDH in the bound state.

2022-06-07 | PXD029364 | Pride

Global analysis of off-target genes by GAPDH siRNA

Project description:A GAPDH siRNA was overexpressed in HeLa cells and microarray expression profiling was performed to experimentally identify the off-targets of this siRNA at the transcriptome level. Among all predicted siRNA off-targets by MirTarget2, the majority were downregulated by at least 10% (i.e. less than 90% remaining gene expression). Moreover, more than one fifth were downregulated by at least 30%. The gene knockdown data is consistent with previous observations that siRNA off-targets are generally silenced at a more moderate level as compared to silencing of the single intended target GAPDH siRNA was transfected into HeLa cells, and the unintended off-targets was identified by microarrays 24 hours post transfection.

2013-10-03 | E-GEOD-41924 | biostudies-arrayexpress

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