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Short telomeres trigger epithelial to mesenchymal transition programmes and sensitize to folic acid-induced kidney fibrosis in mice [young vs old]

ABSTRACT: Gene expression profiles of Tert+/+ and generation 3 (G3) Tert-/- male and female mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE162445 | GEO | 2021/01/21

REPOSITORIES: GEO

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Short telomeres trigger epithelial to mesenchymal transition programmes and sensitize to folic acid-induced kidney fibrosis in mice [folic acid]

Project description:Gene expression profiles of Tert+/+ and generation 3 (G3) Tert-/- male an female mice were untretaed or tretaed witth Folic acid.

2021-01-21 | GSE162446 | GEO

Short telomeres trigger epithelial to mesenchymal transition programmes and sensitize to folic acid-induced kidney fibrosis in mice

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

2021-01-21 | GSE162447 | GEO

Short telomeres trigger epithelial to mesenchymal transition programmes and sensitize to folic acid-induced kidney fibrosis in mice [young vs old]

Project description:Short telomeres trigger epithelial to mesenchymal transition programmes and sensitize to folic acid-induced kidney fibrosis in mice [young vs old]

| PRJNA681876 | ENA

Short telomeres trigger epithelial to mesenchymal transition programmes and sensitize to folic acid-induced kidney fibrosis in mice [folic acid]

Project description:Short telomeres trigger epithelial to mesenchymal transition programmes and sensitize to folic acid-induced kidney fibrosis in mice [folic acid]

| PRJNA681880 | ENA

Short telomeres trigger epithelial to mesenchymal transition programmes and sensitize to folic acid-induced kidney fibrosis in mice

Project description:Short telomeres trigger epithelial to mesenchymal transition programmes and sensitize to folic acid-induced kidney fibrosis in mice

| PRJNA681875 | ENA

Therapeutic effects of telomerase in mice with pulmonary fibrosis induced by damage to the lungs and short telomeres

Project description:In our previous study, mice with pulmonary fibrosis induced by a bleomycin insult in the context of short telomeres develop pulmonary fibrosis. By using AAV9 vectors carrying the telomerase Tert gene to treat those mice, we explore the possibility of telomerase gene therapy as a possible treatment for IPF patients carrying short telomeres. To further understand gene expression changes undergoing in ATII cells upon telomerase activation, we isolated ATII cells from pulmonary fibrosis Tert-treated and empty vector-treated lungs at 1 week after AAV9 inoculation by FACS.

2018-01-22 | GSE93869 | GEO

Genomic copy number profiling of different generations of Atm-/-TERT-ER T-cell lymphomas and associated resistant tumors following telomerase inhibition

Project description:Genomic copy numbers of various generations of Atm-/-TERT-ER mice treated with 4-OHT or vehicle were profiled. Genomic copy numbers of transplanted G3 Atm-/-TERT-ER T-cell lymphomas with telomerase or ALT

2012-01-17 | GSE35045 | GEO

Growing old, yet staying young: The role of telomeres in bats' exceptional longevity.

Project description: Not available

| S-EPMC5810611 | biostudies-other

Telomerase subunit TERT regulates MYC stability independent of its role on telomeres (array)

Project description:Constitutively active MYC and reactivated telomerase often co-exist in cancers. While the reactivation of telomerase is thought to be essential for replicative immortality, MYC, in conjunction with co-factors, confers several growth advantages to cancer cells. However, it is unclear which co-factors sustain elevated MYC activity in tumors . Here, we identify TERT, the catalytic subunit of telomerase, as a novel regulator of MYC stability in cancers. Binding of TERT to MYC stabilizes its levels on chromatin, contributing to either activation or repression of its target genes. Mechanistically, TERT regulates MYC ubiquitination and stability, and this effect of TERT is independent of its role on telomeres. Genetic inhibition and knocking out of TERT phenocopied the loss of MYC, resulting in reduced disease burden of early- and late-stage MYC-driven murine lymphomas. Conversly, the ectopic expression of TERT could substitute for reduced MYC in these functions. Finally we show that TERT null mice, unlike Terc null mice, show delayed onset of MYC induced lymphomagenesis. Accordingly, inhibiting TERT function in primary human leukemia cells blocked the expression of MYC targets, while Terc depletion had no effects . Based on our data, we conclude that the re-expression of TERT, a direct MYC target in tumors, provides a feed-forward mechanism to potentiate MYC-dependent oncogenesis. P493 cells were stably infected with the following viruses: pLKO shControl and pLKO shTERT.

2015-04-23 | E-GEOD-60175 | biostudies-arrayexpress

Telomerase subunit TERT regulates MYC stability independent of its role on telomeres (ChIP-Seq)

Project description:Constitutively active MYC and reactivated telomerase often co-exist in cancers. While the reactivation of telomerase is thought to be essential for replicative immortality, MYC, in conjunction with co-factors, confers several growth advantages to cancer cells. However, it is unclear which co-factors sustain elevated MYC activity in tumours . Here, we identify TERT, the catalytic subunit of telomerase, as a novel regulator of MYC stability in cancers. Binding of TERT to MYC stabilizes its levels on chromatin, contributing to either activation or repression of its target genes. Mechanistically, TERT regulates MYC ubiquitination and stability, and this effect of TERT is independent of its role on telomeres. Genetic inhibition and knocking out of TERT phenocopied the loss of MYC, resulting in reduced disease burden of early- and late-stage MYC-driven murine lymphomas. Conversly, the ectopic expression of TERT could substitute for reduced MYC in these functions. Finally we show that TERT null mice, unlike Terc null mice, show delayed onset of MYC induced lymphomagenesis. Accordingly, inhibiting TERT function in primary human leukemia cells blocked the expression of MYC targets, while Terc depletion had no effects . Based on our data, we conclude that the re-expression of TERT, a direct MYC target in tumors, provides a feed-forward mechanism to potentiate MYC-dependent oncogenesis. ChIP was performed using anti-MYC (sc-764) in primary lymphoma cells from Eµ-Myc;Tert -/- mice, Eµ-Myc;Tert +/+ mice, or in P493 cells treated with shTert, P493 shTerc and shControl.

2015-04-23 | E-GEOD-60223 | biostudies-arrayexpress

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