Literature DB >> 22113287

Chromatin immunoprecipitation of mouse embryos.

Anne K Voss1, Mathew P Dixon, Tamara McLennan, Andrew J Kueh, Tim Thomas.   

Abstract

During prenatal development, a large number of different cell types are formed, the vast majority of which contain identical genetic material. The basis of the great variety in cell phenotype and function is the differential expression of the approximately 25,000 genes in the mammalian genome. Transcriptional activity is regulated at many levels by proteins, including members of the basal transcriptional apparatus, DNA-binding transcription factors, and chromatin-binding proteins. Importantly, chromatin structure dictates the availability of a specific genomic locus for transcriptional activation as well as the efficiency, with which transcription can occur. Chromatin immunoprecipitation (ChIP) is a method to assess if chromatin modifications or proteins are present at a specific locus. ChIP involves the cross linking of DNA and associated proteins and immunoprecipitation using specific antibodies to DNA-associated proteins followed by examination of the co-precipitated DNA sequences or proteins. In the last few years, ChIP has become an essential technique for scientists studying transcriptional regulation and chromatin structure. Using ChIP on mouse embryos, we can document the presence or absence of specific proteins and chromatin modifications at genomic loci in vivo during mammalian development. Here, we describe a ChIP technique adapted for mouse embryos.

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Year:  2012        PMID: 22113287     DOI: 10.1007/978-1-61779-376-9_23

Source DB:  PubMed          Journal:  Methods Mol Biol        ISSN: 1064-3745


  5 in total

1.  Pro-apoptotic Bim suppresses breast tumor cell metastasis and is a target gene of SNAI2.

Authors:  D Merino; S A Best; M-L Asselin-Labat; F Vaillant; B Pal; R A Dickins; R L Anderson; A Strasser; P Bouillet; G J Lindeman; J E Visvader
Journal:  Oncogene       Date:  2014-09-29       Impact factor: 9.867

2.  MOZ (MYST3, KAT6A) inhibits senescence via the INK4A-ARF pathway.

Authors:  B N Sheikh; B Phipson; F El-Saafin; H K Vanyai; N L Downer; M J Bird; A J Kueh; R E May; G K Smyth; A K Voss; T Thomas
Journal:  Oncogene       Date:  2015-03-16       Impact factor: 9.867

3.  Loss of TAF8 causes TFIID dysfunction and p53-mediated apoptotic neuronal cell death.

Authors:  Farrah El-Saafin; Maria I Bergamasco; Yunshun Chen; Rose E May; Prabagaran Esakky; Soroor Hediyeh-Zadeh; Mathew Dixon; Stephen Wilcox; Melissa J Davis; Andreas Strasser; Gordon K Smyth; Tim Thomas; Anne K Voss
Journal:  Cell Death Differ       Date:  2022-03-31       Impact factor: 12.067

4.  Inactivation of Zeb1 in GRHL2-deficient mouse embryos rescues mid-gestation viability and secondary palate closure.

Authors:  Marina R Carpinelli; Michael E de Vries; Alana Auden; Tariq Butt; Zihao Deng; Darren D Partridge; Lee B Miles; Smitha R Georgy; Jody J Haigh; Charbel Darido; Simone Brabletz; Thomas Brabletz; Marc P Stemmler; Sebastian Dworkin; Stephen M Jane
Journal:  Dis Model Mech       Date:  2020-03-25       Impact factor: 5.758

5.  MOZ regulates the Tbx1 locus, and Moz mutation partially phenocopies DiGeorge syndrome.

Authors:  Anne K Voss; Hannah K Vanyai; Caitlin Collin; Mathew P Dixon; Tamara J McLennan; Bilal N Sheikh; Peter Scambler; Tim Thomas
Journal:  Dev Cell       Date:  2012-08-23       Impact factor: 12.270

  5 in total

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