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Anti-THRB Mouse Antibody [K5L2]

Catalog No.: F3941

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution
WB1:1000 IHC1:20 IF1:500

Application
WB, IP, IHC, IF

Reactivity
Human, Mouse, Rat

Source
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
52 kDa; 55 kDa

Positive Control	Human Colon tissue; Human Thyroid tissue
Negative Control

Datasheet & SDS

Biological Description

Specificity
THRB Mouse mAb detects endogenous levels of total THRB protein

Clone
K5L2

Synonym(s)
c-erbA-2; c-erbA-beta; ERBA 2; ERBA BETA; ERBA-BETA; MGC126109; MGC126110; Nuclear receptor subfamily 1 group A member 2; oncogene ERBA2; thyroid hormone nuclear receptor beta variant 1; Thyroid hormone receptor beta; thyroid hormone receptor beta 3; thyroid hormone receptor beta2delta; thyroid hormone receptor, beta (avian erythroblastic leukemia

Background
Thyroid hormone receptor beta (THRB) is a ligand-dependent nuclear transcription factor that belongs to the nuclear receptor superfamily and is primarily activated by the thyroid hormone triiodothyronine (T3). As a member of the thyroid hormone receptor family alongside THRA, THRB exists in multiple isoforms generated through alternative splicing and promoter usage, which contribute to its diverse functional roles. THRB comprises four key domains: an N-terminal activation function-1 (AF-1) domain that modulates transcriptional activity, a highly conserved DNA-binding domain (DBD) containing zinc finger motifs for recognizing thyroid hormone response elements (TREs), a hinge region providing flexibility, and a ligand-binding domain (LBD) that binds T3 and mediates interactions with coactivators and corepressors. In the absence of ligand, THRB associates with corepressor complexes such as N-CoR and SMRT to repress target gene transcription. Upon T3 binding, conformational changes in the LBD displace corepressors and recruit coactivators like SRC-1, leading to activation of genes involved in metabolism, development, and differentiation. THRB isoforms show tissue-specific expression patterns, with THRB1 broadly distributed and THRB2 predominantly expressed in the brain, cochlea, retina, and hypothalamus, where it regulates neurodevelopment and sensory functions. THRB critically regulates metabolic rate, cardiovascular health, auditory and visual system development, and maintains hormonal homeostasis through negative feedback on the hypothalamic-pituitary-thyroid axis by modulating thyroid-stimulating hormone (TSH) synthesis. Mutations in the THRB gene result in resistance to thyroid hormone, characterized by elevated circulating thyroid hormones with impaired receptor function, resulting in growth retardation, hearing loss, and metabolic dysfunction.

Background

Thyroid hormone receptor beta (THRB) is a ligand-dependent nuclear transcription factor that belongs to the nuclear receptor superfamily and is primarily activated by the thyroid hormone triiodothyronine (T3). As a member of the thyroid hormone receptor family alongside THRA, THRB exists in multiple isoforms generated through alternative splicing and promoter usage, which contribute to its diverse functional roles. THRB comprises four key domains: an N-terminal activation function-1 (AF-1) domain that modulates transcriptional activity, a highly conserved DNA-binding domain (DBD) containing zinc finger motifs for recognizing thyroid hormone response elements (TREs), a hinge region providing flexibility, and a ligand-binding domain (LBD) that binds T3 and mediates interactions with coactivators and corepressors. In the absence of ligand, THRB associates with corepressor complexes such as N-CoR and SMRT to repress target gene transcription. Upon T3 binding, conformational changes in the LBD displace corepressors and recruit coactivators like SRC-1, leading to activation of genes involved in metabolism, development, and differentiation. THRB isoforms show tissue-specific expression patterns, with THRB1 broadly distributed and THRB2 predominantly expressed in the brain, cochlea, retina, and hypothalamus, where it regulates neurodevelopment and sensory functions. THRB critically regulates metabolic rate, cardiovascular health, auditory and visual system development, and maintains hormonal homeostasis through negative feedback on the hypothalamic-pituitary-thyroid axis by modulating thyroid-stimulating hormone (TSH) synthesis. Mutations in the THRB gene result in resistance to thyroid hormone, characterized by elevated circulating thyroid hormones with impaired receptor function, resulting in growth retardation, hearing loss, and metabolic dysfunction.

References
https://pubmed.ncbi.nlm.nih.gov/20610536/ https://pubmed.ncbi.nlm.nih.gov/14651789/

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

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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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%