Chd1 Antibody [E24E7] | Primary Antibodies

Application: Reactivity: Human

Lane 1: HEK-293T, Lane 2: HEK-293T (KO CHD1), Lane 3: K562

Usage Information

Dilution
WB1:1000 IF1:50 FCM1:500 CHIP1:1300

Application
WB, IF, FCM, ChIP

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
196 kDa 250 kDa,124 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
Chd1 Antibody [E24E7] detects endogenous levels of total Chd1 protein.

Clone
E24E7

Synonym(s)
Chromodomain-helicase-DNA-binding protein 1; CHD1

Background
Chromodomain‑helicase‑DNA‑binding protein 1 (CHD1) is a member of the CHD family of ATP‑dependent chromatin remodelers that couples histone-modification readout to nucleosome restructuring and transcriptional control in euchromatin‑rich regions. CHD1 contains two N‑terminal chromodomains that bind methylated histone H3 at lysine 4 (H3K4me), a central SWI/SNF CTG‑related ATPase module that hydrolyzes ATP to slide, reposition, or evict nucleosomes, and a C‑terminal DNA‑binding region that contributes to DNA‑surface engagement and target‑site selection, enabling CHD1 to maintain open, transcriptionally permissive chromatin at active gene promoters and enhancers. CHD1 binds H3K4‑marked euchromatic loci, promotes nucleosome‑free region formation at promoters, sustains high transcriptional output, and supports the robust activation of lineage‑specific programs during osteoblast differentiation and early embryogenesis, while also coordinating cohesin‑mediated loop boundaries and chromatin topology that influence long‑range enhancer–promoter interactions. CHD1 participates in early damage signaling and chromatin remodeling at break sites, and its ATPase activity helps preserve appropriate histone‑modification landscapes and transcriptional coherence, whereas loss of full‑length CHD1, or of its C‑terminal intrinsically disordered region, impairs condensate‑like assembly of the remodeler with histone‑modifying complexes and non‑coding RNAs, leading to dysregulated gene expression and genome‑instability‑associated tumorigenesis. CHD1 inactivation is recurrent in prostate and other epithelial cancers, where it often co‑occurs with PTEN loss and alters tumor‑microenvironment immune signaling and epigenetic enzyme activity, but germline CHD1 mutations are also associated with neurodevelopmental and intellectual‑disability syndromes.

Background

Chromodomain‑helicase‑DNA‑binding protein 1 (CHD1) is a member of the CHD family of ATP‑dependent chromatin remodelers that couples histone-modification readout to nucleosome restructuring and transcriptional control in euchromatin‑rich regions. CHD1 contains two N‑terminal chromodomains that bind methylated histone H3 at lysine 4 (H3K4me), a central SWI/SNF CTG‑related ATPase module that hydrolyzes ATP to slide, reposition, or evict nucleosomes, and a C‑terminal DNA‑binding region that contributes to DNA‑surface engagement and target‑site selection, enabling CHD1 to maintain open, transcriptionally permissive chromatin at active gene promoters and enhancers. CHD1 binds H3K4‑marked euchromatic loci, promotes nucleosome‑free region formation at promoters, sustains high transcriptional output, and supports the robust activation of lineage‑specific programs during osteoblast differentiation and early embryogenesis, while also coordinating cohesin‑mediated loop boundaries and chromatin topology that influence long‑range enhancer–promoter interactions. CHD1 participates in early damage signaling and chromatin remodeling at break sites, and its ATPase activity helps preserve appropriate histone‑modification landscapes and transcriptional coherence, whereas loss of full‑length CHD1, or of its C‑terminal intrinsically disordered region, impairs condensate‑like assembly of the remodeler with histone‑modifying complexes and non‑coding RNAs, leading to dysregulated gene expression and genome‑instability‑associated tumorigenesis. CHD1 inactivation is recurrent in prostate and other epithelial cancers, where it often co‑occurs with PTEN loss and alters tumor‑microenvironment immune signaling and epigenetic enzyme activity, but germline CHD1 mutations are also associated with neurodevelopmental and intellectual‑disability syndromes.

References
https://pubmed.ncbi.nlm.nih.gov/28475736/ https://pubmed.ncbi.nlm.nih.gov/29529298/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%