ARID1B/BAF250B Antibody [M24N11]

Catalog No.: F4096

Application: Reactivity: Human, Mouse

Lane 1: Jurkat, Lane 2: SH-SY5Y, Lane 3: Neuro-2a

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代表番号: 045-509-1970|電子メール：sales@selleck.co.jp

使用情報

Dilution
WB1:1000 IP1:200

Application
WB, IP

Source
Rabbit Monoclonal Antibody

Reactivity
Human, Mouse

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
250 kDa, 280 kDa

Datasheet & SDS

生物学的記述

Specificity
ARID1B/BAF250B Antibody [M24N11] detects endogenous levels of total ARID1B/BAF250B protein.

Clone
M24N11

Synonym(s)
AT-rich interactive domain-containing protein 1B; ARID domain-containing protein 1B; BAF250B; BRG1-binding protein hELD/OSA1; Osa homolog 2 (hOsa2); p250R; ARID1B; BAF250B; DAN15; KIAA1235; OSA2

Background
ARID1B, also known as BAF250B, is a DNA-binding subunit of the BAF-type SWI/SNF chromatin remodeling complexes. These complexes use ATPase activity from BRG1 or BRM to alter histone-DNA contacts, thereby modulating chromatin accessibility and regulating transcription. ARID1B contains an AT-rich interactive domain (ARID) that enables sequence-specific DNA recognition, as well as a C-terminal region that facilitates subunit assembly. ARID1B and its paralog ARID1A are mutually exclusive within BAF complexes, creating distinct variants with specialized functions. ARID1B recruits BAF complexes to neuronal gene promoters and drives activity-dependent chromatin remodeling essential for dendrite outgrowth, arborization, and synapse maturation during cortical development. This includes upregulation of immediate-early genes such as c-Fos and Arc, which are critical for cytoskeletal dynamics and proper dendritic branching. Loss of ARID1B in hippocampal and cortical pyramidal neurons disrupts these processes, leading to reduced dendritic complexity, abnormal spine morphology, and impaired synaptic transmission. ARID1B is a crucial regulator of neuronal differentiation and plasticity. This makes it a prime target for studies investigating neurodevelopmental wiring and potential therapies aimed at restoring chromatin dynamics in cognitive disorders. Haploinsufficiency, often due to de novo truncating mutations, causes Coffin-Siris syndrome, characterized by intellectual disability, speech impairment, and subtle dysmorphic features, demonstrating the gene’s dosage sensitivity in brain development.

Background

ARID1B, also known as BAF250B, is a DNA-binding subunit of the BAF-type SWI/SNF chromatin remodeling complexes. These complexes use ATPase activity from BRG1 or BRM to alter histone-DNA contacts, thereby modulating chromatin accessibility and regulating transcription. ARID1B contains an AT-rich interactive domain (ARID) that enables sequence-specific DNA recognition, as well as a C-terminal region that facilitates subunit assembly. ARID1B and its paralog ARID1A are mutually exclusive within BAF complexes, creating distinct variants with specialized functions. ARID1B recruits BAF complexes to neuronal gene promoters and drives activity-dependent chromatin remodeling essential for dendrite outgrowth, arborization, and synapse maturation during cortical development. This includes upregulation of immediate-early genes such as c-Fos and Arc, which are critical for cytoskeletal dynamics and proper dendritic branching. Loss of ARID1B in hippocampal and cortical pyramidal neurons disrupts these processes, leading to reduced dendritic complexity, abnormal spine morphology, and impaired synaptic transmission. ARID1B is a crucial regulator of neuronal differentiation and plasticity. This makes it a prime target for studies investigating neurodevelopmental wiring and potential therapies aimed at restoring chromatin dynamics in cognitive disorders. Haploinsufficiency, often due to de novo truncating mutations, causes Coffin-Siris syndrome, characterized by intellectual disability, speech impairment, and subtle dysmorphic features, demonstrating the gene’s dosage sensitivity in brain development.

References
[1] Ka M, et al. J Neurosci. 2016 Mar 2;36(9):2723-42. [2] Santen GW, et al. Nat Genet. 2012 Mar 18;44(4):379-80.

PVDFメンブレン孔径参考表

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%