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JNK pathway blockade promotes HER2-driven breast cancer

ABSTRACT: JNK knockout cells proliferate more and forms bigger mulit acinar sturctures under normal conditions on 3D culture.

ORGANISM(S): Homo sapiens

PROVIDER: GSE196001 | GEO | 2022/12/21

REPOSITORIES: GEO

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JNK pathway blockade promotes HER2-driven breast cancer [RNA-seq]

Project description:JNK knockout cells proliferate more and forms bigger mulit acinar sturctures under normal conditions on 3D culture.

2022-12-21 | GSE196459 | GEO

JNK pathway blockade promotes HER2-driven breast cancer [RNA-seq_primary_mammary_tumor_cell_lines]

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2022-12-21 | GSE200521 | GEO

JNK pathway blockade promotes HER2-driven breast cancer

Project description:JNK pathway blockade promotes HER2-driven breast cancer

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JNK pathway blockade promotes HER2-driven breast cancer [RNA-seq_primary_mammary_tumor_cell_lines]

Project description:JNK pathway blockade promotes HER2-driven breast cancer [RNA-seq_primary_mammary_tumor_cell_lines]

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JNK pathway blockade promotes HER2-driven breast cancer [RNA-seq]

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Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [ChIP-seq]

Project description:Because spermatogonial stem cells (SSCs) are virtually immortal by serial transplantation, SSC decrease in aged testes is considered to be caused by deteriorated microenvironment. Here we report cell-intrinsic mode of SSC aging. SSCs cultured for 5 years proliferate more actively than young SSCs and showed enhanced glycolytic activity but remain euploid and exhibited stable androgenetic imprinting patterns. Moreover, the aged SSCs kept constant SSC activity despite shortened telomeres. The increased proliferative activity of aged SSCs was caused by Wnt7b expression, which likely occurred due to decreased polycomb complex2 activity. Aberrant Wnt7b expression not only decreased reactive oxygen species levels and mitochondria activity but also stimulated glycolysis via c-jun N-terminal kinase (JNK) activation. Analysis of SSCs in Klotho aging mouse model also confirmed hyperactivation of JNK pathway and increased glycolysis. Therefore, not only SSC microenvironment but also intrinsic activation of Wnt7b-mediated glycolysis plays important roles in SSC aging.

2019-07-30 | GSE120777 | GEO

Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [Bisulfite-seq]

2019-07-30 | GSE120775 | GEO

JNK-dependent genes_rVSMC

Project description:Oxidative stress-dependent genes are defined as those induced or suppressed by H2O2 treatement in rat vascular smooth muscle cells. JNK-induced genes in rat vascular smooth muscle cells are defined as those induced by adenoviruses encoding constitutively active MKK7 (caMKK7) + wild type JNK1 (wtJNK1) and suppressed by adenovirus encoding dominant negative JNK1 (APF). JNK-suppressed genes in rat vascular smooth muscle cells are defined as those suppressed by adenoviruses encoding constitutively active MKK7 (caMKK7) + wild type JNK1 (wtJNK1) and induced by adenovirus encoding dominant negative JNK1 (APF). Adenovirus encoding nuclear localizing GFP was used as a control. Keywords = vascular smooth muscle Keywords = hydrogen peroxide Keywords = c-Jun N-terminal kinase Keywords = JNK Keywords = adenovirus Keywords = oxidative stress Keywords: repeat sample

2005-11-09 | GSE2190 | GEO

JNK signalling regulates self-renewal of proliferative urine-derived renal progenitor cells via inhibition of ferroptosis.

Project description:With a global increase in chronic kidney disease patients, alternatives to dialysis and organ transplantation are needed. Stem cell-based therapies could be one possibility to treat chronic kidney disease. Here, we used multipotent urine-derived renal progenitor cells (UdRPCs) to study nephrogenesis. UdRPCs treated with the JNK inhibitor- AEG3482, displayed decreased proliferation and downregulated transcription of cell cycle-associated genes as well as the kidney progenitor markers -SIX2, CITED1, and SALL1. In addition, levels of activated SMAD2/3, which is associated with the maintenance of self-renewal in UdRPCs, were decreased. JNK inhibition resulted in less efficient oxidative phosphorylation and more lipid peroxidation via ferroptosis- an iron-dependent non-apoptotic cell death pathway linked to various forms of kidney disease. Our study reveals the importance of JNK signalling in maintaining self-renewal as well as protection against ferroptosis in SIX2-positive UdRPCs. We propose that UdRPCs can be used for modelling ferroptosis-induced kidney diseases.

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JNK-mediated control of gene expression in liver

Project description:RNAseq analysis of gene expression in Liver of Control and JNK deficient mice fed a control or a High fat diet Contro(Albcre+)l and mice with liver-specific defiency of JNK (Alb Cre+ Jnk1flox/flox, Jnk2flox/flox or Jnk1flox/floxJnk2flox/flox) were fed a control or a high fat diet for 16 weeks. Gene expression analysis in liver was analyzed by RNAseq

2015-03-06 | E-GEOD-55190 | biostudies-arrayexpress

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