Similar Datasets
Project description:JNK knockout cells proliferate more and forms bigger mulit acinar sturctures under normal conditions on 3D culture.
2022-12-21 | GSE196001 | GEO
Project description:JNK deletion in MMTV-NIC mouse model promotes mammary gland tumor formation.
2022-12-21 | GSE200521 | GEO
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
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 | GSE120775 | GEO
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
Project description:Members of the JNK pathway have been found to be mutated in human breast cancer. Mouse studies examining JNK loss in different tissues have demonstrated that the JNK pathway can play a role in cancer. Using and autochthonous mouse model, we found that JNK deficiency on a p53-null background resulted in more rapid tumor onset. To learn more about these tumors we generated cells lines and performed various in vitro assays, as well as RNAseq in hope of finding differentially expressed genes that may explain the differences we observed in vivo.
2018-05-29 | GSE92560 | GEO
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
Project description:Signaling mediates cellular responses to extracellular stimuli. The c-Jun NH2-terminal kinase (JNK) pathway exemplifies one sub-group of Mitogen-activated protein (MAP) kinases, which besides established functions in stress response, also contributes to developmental processes by an unknown mechanism 1-4. Here we show by genome-wide location analysis that JNK binds directly to a large set of active promoters during differentiation of stem cells to neurons. Bound promoters are not enriched for the canonical AP?1 target sites yet for binding motifs for the transcription factor NF?Y. NF-Y indeed occupies these predicted sites genome-wide in vivo and overexpression of a dominant-negative form of NF?YA reduces JNK presence on chromatin. Histone H3 is a substrate for JNK kinase activity in vitro and JNK bound promoters are preferentially enriched for Histone H3 phosphorylated at Serine 10. Inhibition of JNK signaling in postmitotic neurons reduces this chromatin phosphorylation as well as expression of target genes. Together this establishes MAP kinase binding and function on chromatin at a novel class of target genes during stem cell differentiation. Our Dataset comprises 5 ChIP-seq samples using chromatin from ES, NP and TN cells which was immunoprecipitated, using antibodies against H3K27me3, H3K4me2, RNA Pol II, JNK1/3 and NF-YA. From the same cells we generated biological replicates of RNA-seq data.
2011-12-18 | E-GEOD-25532 | biostudies-arrayexpress
Project description:We found that transient inhibition of JNK pathway increased short term-HSC frequency in cord blood CD34+ cells by 12.56 folds. Transcriptome analysis shows that inhibition of JNK pathway upregulated HSC-specific and anti-oxidative gene expression, prevented upregulation of cell cycle entry, oxidative phosphorylation and glycolysis related gene expression, and downregulated reactive oxygen species (ROS) active gene expression. Consistently, cell cycle and metabolic analysis show that inhibition of JNK pathway prevented HSC from cell cycle entry, glucose uptake increase and ROS accumulation. Accordingly, transient inhibition of JNK pathway also enhanced long term-HSC recovery during cord blood CD34+ cell collection. Collectively, these findings suggest that transient inhibition of JNK pathway could promote quiescent state of HSCs by preventing cell cycle entry and metabolic activation, thus improving HSC recovery and engraftment ability.
2022-06-29 | GSE165501 | GEO
Project description:Signaling mediates cellular responses to extracellular stimuli. The c-Jun NH2-terminal kinase (JNK) pathway exemplifies one sub-group of Mitogen-activated protein (MAP) kinases, which besides established functions in stress response, also contributes to developmental processes by an unknown mechanism 1-4. Here we show by genome-wide location analysis that JNK binds directly to a large set of active promoters during differentiation of stem cells to neurons. Bound promoters are not enriched for the canonical AP?1 target sites yet for binding motifs for the transcription factor NF?Y. NF-Y indeed occupies these predicted sites genome-wide in vivo and overexpression of a dominant-negative form of NF?YA reduces JNK presence on chromatin. Histone H3 is a substrate for JNK kinase activity in vitro and JNK bound promoters are preferentially enriched for Histone H3 phosphorylated at Serine 10. Inhibition of JNK signaling in postmitotic neurons reduces this chromatin phosphorylation as well as expression of target genes. Together this establishes MAP kinase binding and function on chromatin at a novel class of target genes during stem cell differentiation.
2011-12-18 | GSE25532 | GEO