REST Antibody [G10D4] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat, Monkey

Lane 1: Hela, Lane 2: NIH/3T3, Lane 3: C6, Lane 4: COS

Usage Information

Dilution
WB1:1000 CHIP1:50

Application
WB, ChIP

Reactivity
Human, Mouse, Rat, Monkey

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
200 kDa

Positive Control	HeLa cells; NIH/3T3 cells; C6 cells; COS-7 cells
Negative Control

Datasheet & SDS

Biological Description

Specificity
REST Antibody [G10D4] detects endogenous levels of total REST protein.

Clone
G10D4

Synonym(s)
RE1-silencing transcription factor; Neural-restrictive silencer factor; X2 box repressor; REST; NRSF; XBR

Background
REST (RE1-silencing transcription factor), also known as NRSF, functions as a master transcriptional repressor that silences neuronal differentiation genes in non-neuronal cells and stem cells by binding neuron-restrictive silencer elements (NRSE/RE1) through its central zinc-finger DNA-binding domain comprising eight C2H2 tandem zinc fingers that recognize a 21-bp core motif (CACCCNNGGCAG) in an anti-parallel configuration with conformational flexibility, flanked by N-terminal RD1 and C-terminal RD2 repression domains plus lysine/proline-rich regions that recruit the CoREST complex (LSD1, HDAC1/2, Sin3A, MeCP2) for epigenetic silencing, alongside a lysine-rich NLS for nuclear localization. REST/CoREST nucleates local chromatin compaction via H3K9/27 methylation, nucleosome phasing shifts, and long-range looping to block enhancer-promoter contacts (inhibiting PCDHα HS5-1 enhancer via CTCF displacement), while regulating miRNA biogenesis (pri-miR processing via Drosha/DGCR8) and lncRNAs in feedback loops that maintain neural progenitor self-renewal; REST degradation during differentiation, via GSK3β phosphorylation and SCF-βTrCP ubiquitination, derepresses >2000 neuronal targets, including synaptophysin, β-III tubulin, and Nav channels, to enable neurogenesis. REST hyperactivation drives medulloblastoma, neuroblastoma, and Wilms tumor progression by enforcing stemness and blocking differentiation, while nuclear loss in Alzheimer's (via pathology-induced degradation) impairs neuroprotection and memory consolidation; REST polymorphisms associate with Huntington's chorea onset and schizophrenia susceptibility through dysregulated neuronal gene networks.

Background

REST (RE1-silencing transcription factor), also known as NRSF, functions as a master transcriptional repressor that silences neuronal differentiation genes in non-neuronal cells and stem cells by binding neuron-restrictive silencer elements (NRSE/RE1) through its central zinc-finger DNA-binding domain comprising eight C2H2 tandem zinc fingers that recognize a 21-bp core motif (CACCCNNGGCAG) in an anti-parallel configuration with conformational flexibility, flanked by N-terminal RD1 and C-terminal RD2 repression domains plus lysine/proline-rich regions that recruit the CoREST complex (LSD1, HDAC1/2, Sin3A, MeCP2) for epigenetic silencing, alongside a lysine-rich NLS for nuclear localization. REST/CoREST nucleates local chromatin compaction via H3K9/27 methylation, nucleosome phasing shifts, and long-range looping to block enhancer-promoter contacts (inhibiting PCDHα HS5-1 enhancer via CTCF displacement), while regulating miRNA biogenesis (pri-miR processing via Drosha/DGCR8) and lncRNAs in feedback loops that maintain neural progenitor self-renewal; REST degradation during differentiation, via GSK3β phosphorylation and SCF-βTrCP ubiquitination, derepresses >2000 neuronal targets, including synaptophysin, β-III tubulin, and Nav channels, to enable neurogenesis. REST hyperactivation drives medulloblastoma, neuroblastoma, and Wilms tumor progression by enforcing stemness and blocking differentiation, while nuclear loss in Alzheimer's (via pathology-induced degradation) impairs neuroprotection and memory consolidation; REST polymorphisms associate with Huntington's chorea onset and schizophrenia susceptibility through dysregulated neuronal gene networks.

References
https://pubmed.ncbi.nlm.nih.gov/29351877/ https://pubmed.ncbi.nlm.nih.gov/18959480/

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%