Hsp60 gene sequence
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB30885 | ENA |
REPOSITORIES: ENA
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Project description:Pro-inflammatory response of VSMCs is triggered by endothelial damage and a causative step for thrombosis and neointimal thickening in the arterial vessels. Therefore, we investigate a role of cytosolic Hsp60 as a novel pro-inflammatory mediator in VSMCs. Hsp60 was detected in the cytosol of VSMCs. The selective depletion of cytosolic Hsp60 in VSMCs reduced the IKK activation, repressed the induction of NF-κB-dependent pro-survival genes (MnSOD and Bfl-1/A1), and enhanced apoptotic death in response to TNF-α. Moreover, a quantitative RNA sequencing revealed that the expression of 75 genes among the 774 TNF-α-inducible genes was significantly reduced by the depletion of cytosolic Hsp60. In particular, the expression of pro-inflammatory cytokines/chemokines, such as CCL2, CCL20, and IL-6, was regulated by the cytosolic Hsp60 in VSMCs. Finally, the depletion of cytosolic Hsp60 markedly inhibited the neointimal thickening in the balloon-injured arterial vessels by inducing apoptotic cell death and inhibiting chemokine production. This study provides the first evidence that cytosolic Hsp60 could be a therapeutic target for preventing inflammation-driven VSMC hyperplasia in the injured vessels. Hsp60 normal vs knockout with TNF-alpha treatment
2015-03-01 | E-GEOD-65354 | biostudies-arrayexpress
Project description:Pro-inflammatory response of VSMCs is triggered by endothelial damage and a causative step for thrombosis and neointimal thickening in the arterial vessels. Therefore, we investigate a role of cytosolic Hsp60 as a novel pro-inflammatory mediator in VSMCs. Hsp60 was detected in the cytosol of VSMCs. The selective depletion of cytosolic Hsp60 in VSMCs reduced the IKK activation, repressed the induction of NF-κB-dependent pro-survival genes (MnSOD and Bfl-1/A1), and enhanced apoptotic death in response to TNF-α. Moreover, a quantitative RNA sequencing revealed that the expression of 75 genes among the 774 TNF-α-inducible genes was significantly reduced by the depletion of cytosolic Hsp60. In particular, the expression of pro-inflammatory cytokines/chemokines, such as CCL2, CCL20, and IL-6, was regulated by the cytosolic Hsp60 in VSMCs. Finally, the depletion of cytosolic Hsp60 markedly inhibited the neointimal thickening in the balloon-injured arterial vessels by inducing apoptotic cell death and inhibiting chemokine production. This study provides the first evidence that cytosolic Hsp60 could be a therapeutic target for preventing inflammation-driven VSMC hyperplasia in the injured vessels.
2015-03-01 | GSE65354 | GEO
Project description:Here, we profiled the transcriptional capacity of a library of regulatory sequences mined from diverse Biosynthetic Gene Clusters in S. albidoflavus (S. albus J1074) to investigate BGC gene regulation.
2022-06-07 | E-MTAB-9223 | biostudies-arrayexpress
Project description:To identify regulatory responses that could give clues as to the cause(s) of the growth arrest observed in E. coli cells expressing mutant Hsp60-(p.Val98Ile) and Hsp10 versus cells expressing wild type Hsp60 and Hsp10, we performed microarray analyses. We reasoned that the decreased chaperonin activity of the Hsp60-(p.Val98Ile) protein would greatly impair or abolish folding of E. coli proteins that depend on chaperonin assistance. The resulting decreased levels of various activities may cause compensatory up-regulation or deregulation of genes. The transcriptomes of cells shifted to expression of the arabinose-inducible chaperonin operon with either the Hsp60-(p.Val98Ile) mutant or the wild type Hsp60 from the second plasmid were compared. RNA samples from three independent cultures expressing the mutant or two independent cultures expressing wild type Hsp60 were pooled, respectively. Keywords: Comparison of cells expressing two different variants of Hsp60
2008-04-14 | GSE10974 | GEO
Project description:To date there is no clear explanation as to how Chlamydia pneumoniae heat shock protein 60 (cHSP60) gets activated either through TLR-2/4, MAPKinase (p38/JNK/ERK), apoptotic/antiapoptotic, chemokines and inflammatory cytokines pathways leading to coronary artery disease (CAD). Hence to better understanding towards cHSP60 signaling in CAD patients, we performed experiments at RNA levels in cHSP60 positive and negative groups of CAD patients. For the determination of positivity for C. pneumoniae, Helicobacter pylori, Cytomegalovirus and Herpes Simplex Virus in atheromatous plaque multiplex Real Time PCR was performed. Monoplex Real Time PCR was also performed with 16S rRNA and HSP60 gene Chlamydia pneumoniae. Further study was performed only on cHSP60 positive (negative for H. pylori, CMV & HSV-1) and cHSP60 negative (also negative for H. pylori, CMV & HSV-1) CAD patients.
2010-01-06 | GSE19590 | GEO
Project description:To identify regulatory responses that could give clues as to the cause(s) of the growth arrest observed in E. coli cells expressing mutant Hsp60-(p.Val98Ile) and Hsp10 versus cells expressing wild type Hsp60 and Hsp10, we performed microarray analyses. We reasoned that the decreased chaperonin activity of the Hsp60-(p.Val98Ile) protein would greatly impair or abolish folding of E. coli proteins that depend on chaperonin assistance. The resulting decreased levels of various activities may cause compensatory up-regulation or deregulation of genes. The transcriptomes of cells shifted to expression of the arabinose-inducible chaperonin operon with either the Hsp60-(p.Val98Ile) mutant or the wild type Hsp60 from the second plasmid were compared. RNA samples from three independent cultures expressing the mutant or two independent cultures expressing wild type Hsp60 were pooled, respectively. Experiment Overall Design: B178 (groELS)-deleted cells double-transformed with two plasmids harboring an IPTG-inducible operon with wild type human Hsp60 and Hsp10 and a second plasmid harboring an arabinose inducible operon with either Hsp60-(p.Val98Ile) and Hsp10 (mutant cells) or wild type Hsp60 and Hsp10 (wild type cells) were grown in dYT medium (21) supplemented with kanamycin (10 mg/L), ampicillin (100 mg/L) and IPTG (0.1mM) at 30°C in a shaking water bath. At OD536 â?? 0.1 bacteria were harvested by centrifugation at ambient temperature, resuspended in fresh medium, and 0.2% arabinose was added. Growth was continued at 30°C. After 10 hours 3ml samples were withdrawn and RNA was isolated. Experiment Overall Design: Two independent transformant clones of the wild type cells and three of the mutant cells were grown in this way. The RNA preps from the 2 wild type and the three mutant cells, respectively, were pooled, cDNA was synthesized, labelled and subjected to Affymetrix arrays.
2008-06-11 | E-GEOD-10974 | biostudies-arrayexpress
Project description:Specific DNA-protein interactions mediate physiologic gene regulation and may be altered by DNA variants linked to polygenic disease. To enhance the speed and signal-to-noise ratio (SNR) of identifying and quantifying proteins associating with specific DNA sequences in living cells, we developed proximal biotinylation by episomal recruitment (PROBER). PROBER uses high copy episomes to amplify SNR along with proximity proteomics (BioID) to identify the transcription factors (TFs) and additional gene regulators associated with DNA sequences of interest. PROBER quantified steady-state and inducible association of TFs and associated chromatin regulators to target DNA sequences and quantified binding quantitative trait loci (bQTLs) due to single nucleotide variants. PROBER identified alterations in gene regulator associations due to cancer hotspot mutations in the hTERT promoter, indicating these mutations increase promoter association with specific gene activators. PROBER offers an approach to rapidly identify proteins associated with specific DNA sequences and their variants in living cells.
2022-07-27 | PXD023732 | Pride
Project description:DNA-protein interactions mediate physiologic gene regulation and may be altered by DNA variants linked to polygenic disease. To enhance the speed and signal-to-noise ratio (SNR) of identifying and quantifying proteins that associate with specific DNA sequences in living cells, we developed proximal biotinylation by episomal recruitment (PROBER). PROBER uses high copy episomes to amplify SNR along with proximity proteomics (BioID) to identify the transcription factors (TFs) and additional gene regulators associated with short DNA sequences of interest. PROBER quantified steady-state and inducible association of TFs and corresponding chromatin regulators to target DNA sequences as well as binding quantitative trait loci (bQTLs) due to single nucleotide variants. PROBER identified alterations in regulator associations due to cancer hotspot mutations in the hTERT promoter, indicating these mutations increase promoter association with specific gene activators. PROBER provides an approach to rapidly identify proteins associated with specific DNA sequences and their variants in living cells
2022-07-27 | PXD032726 | Pride