SIN3A Antibody [B10N4] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution
WB1:1000 IP1:30 FCM1:500

Application
WB, IP, FCM

Reactivity
Human, Mouse, Rat

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
145 kDa 170 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
SIN3A Antibody [B10N4] detects endogenous levels of total SIN3A protein.

Clone
B10N4

Synonym(s)
Paired amphipathic helix protein Sin3a, Histone deacetylase complex subunit Sin3a, Transcriptional corepressor Sin3a, SIN3A

Background
mSin3A is a key scaffolding protein of the Sin3 transcriptional corepressor complex that regulates gene silencing and chromatin organization through recruitment of histone deacetylases (HDACs) despite lacking intrinsic DNA-binding activity. mSin3A contains multiple paired amphipathic helix (PAH) domains that mediate interactions with diverse transcriptional repressors such as REST, Mad-Max, and p53, while simultaneously associating with HDAC1/2, RbAp48, SAP proteins, and other chromatin regulators to assemble a stable multiprotein repression complex. Through these interactions, mSin3A bridges sequence-specific transcription factors to HDAC activity at promoters of genes involved in cell cycle regulation, differentiation, apoptosis, and development, leading to histone H3 and H4 deacetylation, chromatin compaction, and transcriptional repression. In Notch signaling, mSin3A cooperates with CSL-associated repressors to maintain low basal expression of target genes such as Hes1 until pathway activation displaces the repressor complex, whereas during p53-mediated stress responses, mSin3A enhances repression of survival genes, including Bcl2, by promoting local chromatin condensation at p53-bound promoters. mSin3A plays essential roles in cortical neurogenesis by suppressing premature neuronal differentiation programs in neural progenitor cells, thereby coordinating the transition between proliferation and maturation, while loss of mSin3A in embryonic fibroblasts results in derepression of E2F target genes, cell cycle abnormalities, and resistance to apoptosis. Conserved PAH domains together with the C-terminal region provide multiple protein interaction surfaces necessary for assembly and regulation of Sin3 complexes. Dysregulation of mSin3A contributes to human disease, as SIN3A haploinsufficiency is associated with Witteveen-Kolk syndrome characterized by neurodevelopmental delay and intellectual disability, whereas reduced mSin3A expression in breast cancer has been linked to increased tumor invasion and progression.

Background

mSin3A is a key scaffolding protein of the Sin3 transcriptional corepressor complex that regulates gene silencing and chromatin organization through recruitment of histone deacetylases (HDACs) despite lacking intrinsic DNA-binding activity. mSin3A contains multiple paired amphipathic helix (PAH) domains that mediate interactions with diverse transcriptional repressors such as REST, Mad-Max, and p53, while simultaneously associating with HDAC1/2, RbAp48, SAP proteins, and other chromatin regulators to assemble a stable multiprotein repression complex. Through these interactions, mSin3A bridges sequence-specific transcription factors to HDAC activity at promoters of genes involved in cell cycle regulation, differentiation, apoptosis, and development, leading to histone H3 and H4 deacetylation, chromatin compaction, and transcriptional repression. In Notch signaling, mSin3A cooperates with CSL-associated repressors to maintain low basal expression of target genes such as Hes1 until pathway activation displaces the repressor complex, whereas during p53-mediated stress responses, mSin3A enhances repression of survival genes, including Bcl2, by promoting local chromatin condensation at p53-bound promoters. mSin3A plays essential roles in cortical neurogenesis by suppressing premature neuronal differentiation programs in neural progenitor cells, thereby coordinating the transition between proliferation and maturation, while loss of mSin3A in embryonic fibroblasts results in derepression of E2F target genes, cell cycle abnormalities, and resistance to apoptosis. Conserved PAH domains together with the C-terminal region provide multiple protein interaction surfaces necessary for assembly and regulation of Sin3 complexes. Dysregulation of mSin3A contributes to human disease, as SIN3A haploinsufficiency is associated with Witteveen-Kolk syndrome characterized by neurodevelopmental delay and intellectual disability, whereas reduced mSin3A expression in breast cancer has been linked to increased tumor invasion and progression.

References
https://pubmed.ncbi.nlm.nih.gov/16055712/ https://pubmed.ncbi.nlm.nih.gov/15998811/

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%