scholarly journals ChIPprimersDB: a public repository of verified qPCR primers for chromatin immunoprecipitation (ChIP)

2018 ◽  
Vol 47 (D1) ◽  
pp. D46-D49 ◽  
Author(s):  
Stefan Kurtenbach ◽  
Rohit Reddy ◽  
J William Harbour
Keyword(s):  
Chromatin Immunoprecipitation ◽  
Public Repository

Chromatin immunoprecipitation (ChIP) assay

2009 ◽  
Author(s):  
Zhongfu Ni ◽  
Danny W.-K. Ng ◽  
Jianxin Liu ◽  
Z. Jeffrey Chen
Keyword(s):  
Chromatin Immunoprecipitation ◽  
Chip Assay

scholarly journals Efficient automated localization of ECoG electrodes in CT images via shape analysis

2021 ◽  
Vol 16 (4) ◽  
pp. 543-554
Author(s):  
Jessica Centracchio ◽  
Antonio Sarno ◽  
Daniele Esposito ◽  
Emilio Andreozzi ◽  
Luigi Pavone ◽  
...  
Keyword(s):  
Shape Analysis ◽  
Focal Epilepsy ◽  
Support Vector ◽  
Epileptogenic Zone ◽  
Platinum Electrodes ◽  
Public Repository ◽  
Automated Method ◽  
Depth Electrodes ◽  
Ethical Approval ◽  
Cortical Regions

Abstract Purpose People with drug-refractory epilepsy are potential candidates for surgery. In many cases, epileptogenic zone localization requires intracranial investigations, e.g., via ElectroCorticoGraphy (ECoG), which uses subdural electrodes to map eloquent areas of large cortical regions. Precise electrodes localization on cortical surface is mandatory to delineate the seizure onset zone. Simple thresholding operations performed on patients’ computed tomography (CT) volumes recognize electrodes but also other metal objects (e.g., wires, stitches), which need to be manually removed. A new automated method based on shape analysis is proposed, which provides substantially improved performances in ECoG electrodes recognition. Methods The proposed method was retrospectively tested on 24 CT volumes of subjects with drug-refractory focal epilepsy, presenting a large number (> 1700) of round platinum electrodes. After CT volume thresholding, six geometric features of voxel clusters (volume, symmetry axes lengths, circularity and cylinder similarity) were used to recognize the actual electrodes among all metal objects via a Gaussian support vector machine (G-SVM). The proposed method was further tested on seven CT volumes from a public repository. Simultaneous recognition of depth and ECoG electrodes was also investigated on three additional CT volumes, containing penetrating depth electrodes. Results The G-SVM provided a 99.74% mean classification accuracy across all 24 single-patient datasets, as well as on the combined dataset. High accuracies were obtained also on the CT volumes from public repository (98.27% across all patients, 99.68% on combined dataset). An overall accuracy of 99.34% was achieved for the recognition of depth and ECoG electrodes. Conclusions The proposed method accomplishes automated ECoG electrodes localization with unprecedented accuracy and can be easily implemented into existing software for preoperative analysis process. The preliminary yet surprisingly good results achieved for the simultaneous depth and ECoG electrodes recognition are encouraging. Ethical approval n°NCT04479410 by “IRCCS Neuromed” (Pozzilli, Italy), 30th July 2020.

scholarly journals SAA1 is upregulated in gastric cancer-associated fibroblasts possibly by its enhancer activation

2020 ◽  
Author(s):  
Yoshimi Yasukawa ◽  
Naoko Hattori ◽  
Naoko Iida ◽  
Hideyuki Takeshima ◽  
Masahiro Maeda ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Chromatin Immunoprecipitation ◽  
Therapeutic Target ◽  
Cancer Associated Fibroblasts ◽  
Promoting Effect ◽  
Gastric Cancer Cells ◽  
Potential Therapeutic Target ◽  
Active Enhancer ◽  
Serum Amyloid A1

Abstract Cancer-associated fibroblasts (CAFs) tend to have tumor-promoting capacity, and can provide therapeutic targets. Even without cancer cells, CAF phenotypes are stably maintained, and DNA methylation and H3K27me3 changes have been shown to be involved. Here, we searched for a potential therapeutic target in primary CAFs from gastric cancer and a mechanism for its dysregulation. Expression microarray using eight CAFs and seven non-CAFs (NCAFs) revealed that serum amyloid A1 (SAA1), which encodes an acute phase secreted protein, was second most upregulated in CAFs, following IGF2. Conditioned medium (CM) derived from SAA1-overexpressing NCAFs was shown to increase migration of gastric cancer cells compared to that from control NCAFs, and its tumor-promoting effect was comparable to that of CM from CAFs. In addition, increased migration of cancer cells by CM from CAFs was mostly canceled with CM from CAFs with SAA1 knockdown. Chromatin immunoprecipitation (ChIP)-quantitative PCR showed that CAFs had higher levels of H3K27ac, an active enhancer mark, in the promoter and the two far upstream regions of SAA1 than NCAFs. Also, BET bromodomain inhibitors, JQ1 and mivebresib, decreased SAA1 expression and tumor-promoting effects in CAFs, suggesting SAA1 upregulation by enhancer activation in CAFs. Our present data showed that SAA1 is a candidate therapeutic target from gastric CAFs and indicated that increased enhancer acetylation is important for its overexpression.

scholarly journals Binding of an X-Specific Condensin Correlates with a Reduction in Active Histone Modifications at Gene Regulatory Elements

Genetics ◽  
2019 ◽  
Vol 212 (3) ◽  
pp. 729-742 ◽  
Author(s):  
Lena Annika Street ◽  
Ana Karina Morao ◽  
Lara Heermans Winterkorn ◽  
Chen-Yu Jiao ◽  
Sarah Elizabeth Albritton ◽  
...  
Keyword(s):  
Gene Expression ◽  
Histone Modifications ◽  
Chromatin Immunoprecipitation ◽  
Protein Complexes ◽  
Regulatory Elements ◽  
Evolutionarily Conserved ◽  
Chromatin Immunoprecipitation Sequencing ◽  
Gene Regulatory Elements ◽  
Gene Regulatory ◽  
Regulatory Sites

Condensins are evolutionarily conserved protein complexes that are required for chromosome segregation during cell division and genome organization during interphase. In Caenorhabditis elegans, a specialized condensin, which forms the core of the dosage compensation complex (DCC), binds to and represses X chromosome transcription. Here, we analyzed DCC localization and the effect of DCC depletion on histone modifications, transcription factor binding, and gene expression using chromatin immunoprecipitation sequencing and mRNA sequencing. Across the X, the DCC accumulates at accessible gene regulatory sites in active chromatin and not heterochromatin. The DCC is required for reducing the levels of activating histone modifications, including H3K4me3 and H3K27ac, but not repressive modification H3K9me3. In X-to-autosome fusion chromosomes, DCC spreading into the autosomal sequences locally reduces gene expression, thus establishing a direct link between DCC binding and repression. Together, our results indicate that DCC-mediated transcription repression is associated with a reduction in the activity of X chromosomal gene regulatory elements.

scholarly journals Two Sides of the Same Coin: TFIIH Complexes in Transcription and DNA Repair

2010 ◽  
Vol 10 ◽  
pp. 633-643 ◽  
Author(s):  
Alexander Zhovmer ◽  
Valentyn Oksenych ◽  
Frédéric Coin
Keyword(s):  
Dna Repair ◽  
Western Blotting ◽  
Chromatin Immunoprecipitation ◽  
Transcription Initiation ◽  
Dna Lesions ◽  
Dynamic Composition ◽  
The Core ◽  
Repair Factor ◽  
A New Technique ◽  
Two Sides

TFIIH is organized into a seven-subunit core associated with a three-subunit Cdk-activating kinase (CAK) module. TFIIH has roles in both transcription initiation and DNA repair. During the last 15 years, several studies have been conducted to identify the composition of the TFIIH complex involved in DNA repair. Recently, a new technique combining chromatin immunoprecipitation and western blotting resolved the hidden nature of the TFIIH complex participating in DNA repair. Following the recruitment of TFIIH to the damaged site, the CAK module is released from the core TFIIH, and the core subsequently associates with DNA repair factors. The release of the CAK is specifically driven by the recruitment of the DNA repair factor XPA and is required to promote the incision/excision of the damaged DNA. Once the DNA lesions have been repaired, the CAK module returns to the core TFIIH on the chromatin, together with the release of the repair factors. These data highlight the dynamic composition of a fundamental cellular factor that adapts its subunit composition to the cell needs.

Sign in / Sign up

Export Citation Format

Share Document