MABE873

Anti-Chd2, clone 8H3 Antibody

Name: Anti-Chd2, clone 8H3 Antibody
Brand: MM
Price: 532 USD

clone 8H3, from rat

Synonym(s):

SNF2 chromatin remodelling enzyme, Chromodomain Helicase DNA Binding Protein 2, Protein Chd2

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100 μG

$532.00

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About This Item

UNSPSC Code:

12352203

NACRES:

NA.41

eCl@ss:

32160702

Key Documents

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Product Name

Anti-Chd2, clone 8H3 Antibody, clone 8H3, from rat

biological source

rat

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

8H3, monoclonal

species reactivity

mouse, human

technique(s)

ChIP: suitable
immunocytochemistry: suitable
immunoprecipitation (IP): suitable
western blot: suitable

isotype

IgG2aκ

NCBI accession no.

NP_001074814

UniProt accession no.

E9PZM4

shipped in

wet ice

target post-translational modification

unmodified

Quality Level

100

Gene Information

human ... CHD2(1106)

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This Item	MABE455	ABE86	MABE914
Sigma-Aldrich MABE873 Anti-Chd2, clone 8H3 Antibody	Sigma-Aldrich MABE455 Anti-CHD-4 Antibody, clone 3F2/4	Sigma-Aldrich ABE86 Anti-CHD-3 Antibody	Sigma-Aldrich MABE914 Anti-Mi-2β Antibody, clone 16G4
clone 8H3, monoclonal	clone 3F2/4, monoclonal	clone polyclonal	clone 16G4, monoclonal
biological source rat	biological source mouse	biological source rabbit	biological source mouse
Gene Information human ... CHD2(1106)	Gene Information human ... CHD4(1108)	Gene Information human ... CHD3(1107)	Gene Information human ... CHD4(1108)
antibody form purified immunoglobulin	antibody form purified immunoglobulin	antibody form affinity isolated antibody	antibody form purified immunoglobulin
species reactivity mouse, human	species reactivity mouse, human	species reactivity human	species reactivity human
technique(s) ChIP: suitable, immunoprecipitation (IP): suitable, immunocytochemistry: suitable, western blot: suitable	technique(s) ChIP: suitable, immunofluorescence: suitable, immunohistochemistry: suitable, western blot: suitable	technique(s) western blot: suitable	technique(s) ChIP: suitable (ChIP-seq), western blot: suitable

Analysis Note

Evaluated by Western Blotting in Jurkat cell lysate.

Western Blotting Analysis: 1 µg/mL of this antibody detected Chd2 in 10 µg of Jurkat cell lysate.

Application

Immunoprecipitation Analysis: A representative lot from an independent laboratory immunoprecipitated Chd2 from C2C12 cell lysate (Harada, A., et al. (2012). EMBO J. 31(13):2994-3007.).

Immunocytochemistry Analysis: A representative lot from an independent laboratory detected Chd2 in C2C12 cells (Harada, A., et al. (2012). EMBO J. 31(13):2994-3007.).

Chromatin Immunoprecipitation Analysis: A representative lot from an independent laboratory immunoprecipitated Chd2 from C2C12 cell lysate (Harada, A., et al. (2012). EMBO J. 31(13):2994-3007.).

Research Category
Epigenetics & Nuclear Function

Research Sub Category
Chromatin Biology

This Anti-Chd2 antibody, clone 8H3 is validated for use in western blotting, IP, ICC & ChIP for the detection of Chd2.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

General description

Chd2, also known as Chromodomain-helicase-DNA-binding protein 2 (CHD-2), or ATP-dependent helicase CHD2, and encoded by the gene CHD2, belongs to the CHD family of proteins. This family is characterized by the presence of chromo (chromatin organization modifier) domains and SNF2-related helicase/ATPase domains. CHD genes are chromatin remodeling proteins and alter gene expression by modifying the chromatin structure of a particular gene. The alteration affects the access of the transcriptional apparatus to it, and thus the gene’s expression. In the mouse Chd2 is expressed in heart, forebrain, extremities, and facial and dorsal regions during specific times of embryonic development. Chd2 null mice are embryonic lethal, and in humans, various mutations in CHD-2 gene appear to cause a variety of disorders and developmental defects. Other mutations associated with the CHD2 gene locus appear to cause childhood-onset epileptic encephalopathy (EEOC).

~211 kDa observed. Uncharacterized band(s) may be observed in some cell lysates. Two known isoforms may be observed at 50 kDa and 200 kDa

Immunogen

Recombinant protein corresponding to mouse Chd2.

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Physical form

Format: Purified

Protein G Purified

Purified rat monoclonal IgG2aκ in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Preparation Note

Stable for 1 year at 2-8°C from date of receipt.

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Storage Class

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Chromodomain helicase DNA-binding domain 2 maintains spermatogonial self-renewal by promoting chromatin accessibility and mRNA stability.

Ziqian Min et al.

iScience, 25(12), 105552-105552 (2022-11-30)

Chromodomain helicase DNA-binding domain 2 (CHD2) is a chromatin remodeling factor involved in many developmental processes. However, its role in male germ cell development has not been elucidated. Here, we confirm that CHD2 expression is enriched in the male germline.

Regulation of CHD2 expression by the Chaserr long noncoding RNA gene is essential for viability.

Aviv Rom et al.

Nature communications, 10(1), 5092-5092 (2019-11-11)

Chromodomain helicase DNA binding protein 2 (Chd2) is a chromatin remodeller implicated in neurological disease. Here we show that Chaserr, a highly conserved long noncoding RNA transcribed from a region near the transcription start site of Chd2 and on the

Autism-like phenotype and risk gene mRNA deadenylation by CPEB4 mis-splicing.

Alberto Parras et al.

Nature, 560(7719), 441-446 (2018-08-17)

Common genetic contributions to autism spectrum disorder (ASD) reside in risk gene variants that individually have minimal effect sizes. As environmental factors that perturb neurodevelopment also underlie idiopathic ASD, it is crucial to identify altered regulators that can orchestrate multiple

Cancer is a complex disease manifestation. At its core, it remains a disease of abnormal cellular proliferation and inappropriate gene expression. In the early days, carcinogenesis was viewed simply as resulting from a collection of genetic mutations that altered the gene expression of key oncogenic genes or tumor suppressor genes leading to uncontrolled growth and disease (Virani, S et al 2012). Today, however, research is showing that carcinogenesis results from the successive accumulation of heritable genetic and epigenetic changes. Moreover, the success in how we predict, treat and overcome cancer will likely involve not only understanding the consequences of direct genetic changes that can cause cancer, but also how the epigenetic and environmental changes cause cancer (Johnson C et al 2015; Waldmann T et al 2013). Epigenetics is the study of heritable gene expression as it relates to changes in DNA structure that are not tied to changes in DNA sequence but, instead, are tied to how the nucleic acid material is read or processed via the myriad of protein-protein, protein-nucleic acid, and nucleic acid-nucleic acid interactions that ultimately manifest themselves into a specific expression phenotype (Ngai SC et al 2012, Johnson C et al 2015). This review will discuss some of the principal aspects of epigenetic research and how they relate to our current understanding of carcinogenesis. Because epigenetics affects phenotype and changes in epigenetics are thought to be key to environmental adaptability and thus may in fact be reversed or manipulated, understanding the integration of experimental and epidemiologic science surrounding cancer and its many manifestations should lead to more effective cancer prognostics as well as treatments (Virani S et al 2012).

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