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Atg5 knockout down-regulates the KEGG pathway ‘Oxidative Phosphorylation’ in erastin2-treated primary PTECs

ABSTRACT: To explore the mechanisms by which Atg5 deficiency sensitizes PTECs to ferroptosis

ORGANISM(S): Mus musculus

PROVIDER: GSE298268 | GEO | 2025/11/14

REPOSITORIES: GEO

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Atg5 knockout down-regulates the KEGG pathway ‘Oxidative Phosphorylation’ in erastin2-treated primary PTECs

Project description:Atg5 knockout down-regulates the KEGG pathway ‘Oxidative Phosphorylation’ in erastin2-treated primary PTECs

| PRJNA1268769 | ENA

Gene expression analysis of kidney primary tubular epithelial cells (PTECs), SETD2-KD PTECs, PBRM1-KD PTECs and ccRCC derived cell lines

Project description:Transcriptional profiling of human WT-PTECs, SETD2-KD PTECs, PBRM1-KD PTECs, and 10 different ccRCC derived cell lines. ccRCC derived cell lines showed distict expression signatures as compared to PTECs, some of them also present in SETD2-KD PTECs, and/or PBRM1-KD PTECs.

2017-11-01 | GSE89214 | GEO

Gene expression analysis of untreated and NT-shRNA transduced kidney proximal tubular epithelial cells (PTECs) at day 6 and day 16 after transduction, as well as SETD2-shRNA transduced PTECs at day 25 after transduction.

Project description:Primary kidney PTECs gradually became senescesince day 16, but SETD2 depletion prevented PTECs from senescence and maintained their proliferation beyond their limited dividing capacity. Transcriptional profiling of human PTECs, with comparing of non-senescent PTECs (PTECs-day 6), senescent PTECs (PTECs-day16), and SETD2 depleted PTECs at day 25 (SETD2 KD-PTECs-day 25). Three PTECs of different origins were transduced with shRNA constructs against SETD2 (sh1 or sh2), or with a non-targeting sequence. Untreated and NT-shRNA transduced samples were harvest at day 6 and day 16 respectively, SETD2-KD shRNA transduced PTECs were harvest at day 25.

2016-01-09 | E-GEOD-72792 | biostudies-arrayexpress

Project description:Primary kidney PTECs gradually became senescent after a few passages, but SETD2 depletion prevented PTECs from senescence and maintained their proliferation beyond their limited dividing capacity. Transcriptional profiling of human PTECs, with comparing of SETD2 wild-type non-senescent PTECs at day 6 (WT-PTECs-day 6), SETD2 wild-type senescent PTECs at day 16 (WT-PTECs-day16), and SETD2 knockdown PTECs at day 25 (KD-PTECs-day 25).

2016-01-09 | GSE72792 | GEO

Differentially expressed mRNAs with statistical significance in cisplatin treated wild-type PTECs infected with Ad-FXRα2 or Ad-VP16

Project description:We report the application of RNA-sequence in Primary PTECs, by obtaining the sequence from cisplatin treated wild-type PTECs infected with Ad-FXRα2 or Ad-VP16

2020-11-28 | GSE162279 | GEO

Genome-wide expression analysis in Control and Atg5-deficient eosinophils.

Project description:Depletion of autophagy-associated protein 5 (Atg5), specifically within the eosinophil lineage in mice, resulted in increased body weight, impaired glucose metabolism, and structural alterations in adipose tissue. Our findings highlight that Atg5 influences the functional activity of eosinophils within adipose tissue rather than their quantity. To gain a deeper understanding of the molecular mechanisms underlying ATG5's role in eosinophils, we conducted total RNA-seq analyses on control and Atg5-deficient eosinophils isolated from both bone marrow and blood of mice.

2023-11-21 | GSE245134 | GEO

Next Generation Sequencing analysis atg5 gene expression in zebrafish model

Project description:Purpose: study of function of ATG5 protein on zebrafish larvae development Methods: Using morpholino oligos for atg5 gene knock down and overexpression, injected into one- to four-cell-stage embryos,extracted total RNA, then sending to RNA sequencing. Results: we compared to Wildtype, 5MO and atg5 mRNA groups, we analyza autophagy related gene mRNA expression, there are obvious different. Conclusion: our study showed the function of autophagy related gene 5 on zebrafish larvae, it has an important significant for understanding the affection of autophagy on embryo development

2019-04-30 | GSE120170 | GEO

ATG5 suppresses type I interferon-dependent neutrophil swarming and NET release

Project description:Inflammation is critical for controlling infections but can cause disease when unchecked. For tuberculosis, the leading cause of death by infection, neutrophil-dominated inflammation is associated with disease progression, emphasizing the need to understand how neutrophil functions are regulated during Mycobacterium tuberculosis infection. Atg5 was the first gene shown to specifically function within neutrophils to promote control of M. tuberculosis. ATG5 is best studied for its role in autophagy, however, the protective activity of ATG5 in neutrophils was unexpectedly independent of other autophagy proteins and remained elusive. We report that ATG5 is required in neutrophils to suppress type I interferon-induced neutrophil extracellular trap (NET) release and swarming during M. tuberculosis infection. Elevated NET release contributes to the early susceptibility of Atg5fl/fl-LysM-Cre mice during infection. These findings identify ATG5 as a master regulator of how type I interferon influences neutrophil responses during infection, revealing a new potential target for host-directed therapies.

2025-03-07 | GSE280193 | GEO

Autophagy and alternative NF-kappaB inhibition by RNAi against RELB, ATG5 or ULK1 in A549 human cancer cells

Project description:In order to understand the contribution of autophagy and alternative NF-kappaB signalling to transcriptional output in A549 lung cancer cells, RNAi was used to knockdown the expression of core autophagy genes (ATG5, ULK1) or the key subunit of alternative NF-kappaB RELB. Seven samples were prepared for each biological replicate; two sequence independent non-targeting control siRNAs were transfected as a negative control. Three sequence independent siRNAs targeting the core autophagy machinery were transfected (ATG5 si, ATG5 si(2), ULK1 si). N.B. ATG5 si(2) only partially ablates Atg5 protein expression whereas ATG si has greater efficacy. Two sequence independent siRNAs targeting RELB were transfected (RELB si, RELB si(2) ). Three independent biological replicates of all conditions were obtained, by performance of the experiment on different days.

2015-09-18 | E-GEOD-73158 | biostudies-arrayexpress

Identification Atg5-related microRNAs involved in the regulation of tumor formation

Project description:Autophagy plays an important role in physiology and tumorigenesis. We and others have demonstrated that Ha-ras overexpression induces autophagy in NIH3T3 cells. Autophagic machinery is regulated by a family of autophagy associated genes (Atg). The inducible Ha-ras oncogene was introduced into mouse embryo fibroblast Atg5 wild type [MEF-Atg5(+/+)] and Atg5 knock-out [MEF-Atg5(-/-)] cells and the stable cell lines MR and M5R were established, respectively. Our results showed that M5R cell induced larger tumor formation compared with MR cells while these two cell lines were subcutaneously injected into SCID mice under Ha-ras overexpression conditions. It indicates that Atg5 is involved in the suppression of Ras-related tumor formation. MicroRNA (miRNA), approximately 22 nucleotide of non-coding RNA, regulates transcription and translation of the target genes and is involved in cell differentiation and tumorigenesis. A miRNA microarray (932 probes) screening was conducted to identify the autophagy-tumorigenesis-related miRNAs. Among the significant genes, miR-224 was highly expressed in autophagy deficient cell and it induced tumors. Overexpression miR-224 enhanced the activity of migration and invasion in vitro and tumor formation in vivo. In conclusion, this is the first report to demonstrate that autophagy suppresses tumor formation through down-regulation of microRNA in this case miR-224. MR and M5R cell lines were treated with IPTG for 48 hr. In addition, these cell lines were subcutaneously injected into mice to induce tumor formation. The RNA samples were extracted from above cell lines and tumors. In this research, BEL/ITRI 15K V1.0 miRNA microarray chips were used to evaluate the miRNA expression profile.

2012-06-25 | E-GEOD-38911 | biostudies-arrayexpress

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