SR-2A Antibody [L13G15] | Primary Antibodies

Application: Reactivity: Mouse, Rat, Human

Usage Information

Dilution
WB1:100-1:1000 IP1:100-1:200 IHC1:50-1:500 IF1:50-1:500

Application
WB, IP, IHC, IF, ELISA

Reactivity
Mouse, Rat, Human

Source
Mouse 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
55 kDa

Datasheet & SDS

Biological Description

Specificity
SR-2A Antibody [L13G15] detects endogenous levels of total SR-2A protein.

Clone
L13G15

Synonym(s)
5-hydroxytryptamine receptor 2A, 5-HT-2 , 5-HT-2A, Serotonin receptor 2A, HTR2A, HTR2

Background
SR‑2A corresponds to the serotonin 2A receptor (5‑HT2A/HTR2A), a class A G protein‑coupled receptor that is widely expressed in cortex, limbic regions, platelets, and peripheral tissues, where it transduces serotonergic signals into phospholipase C activation, intracellular calcium mobilization, and downstream changes in neuronal excitability, synaptic plasticity, and smooth muscle tone. The receptor has the canonical seven transmembrane helical bundle with extracellular loops contributing to ligand binding, an orthosteric site that accommodates serotonin and a broad range of psychoactive agonists and antagonists, and an intracellular face that couples primarily to Gq/11 proteins, enabling 5‑HT2A to link monoamine neurotransmission to phosphoinositide hydrolysis and IP3/DAG second messenger generation. Activation of 5‑HT2A stimulates PLCβ, leading to IP3‑dependent Ca²⁺ release and DAG‑mediated PKC activation, and also engages β‑arrestin–dependent scaffolding and multiple kinase pathways, including ERK, which together regulate gene expression, receptor desensitization, and long‑term changes in neuronal circuits involved in mood, perception, and cognition. Central 5‑HT2A receptors are highly expressed on pyramidal neurons in prefrontal cortex and other associative areas, where they modulate glutamatergic output and participate in stress and danger‑related responses; stress exposure and glucocorticoid signaling upregulate cortical 5‑HT2A expression and function, supporting the idea that this receptor constitutes part of a stress‑response system that adjusts cortical processing under threat. Dysregulated 5‑HT2A signaling in major depression, schizophrenia, and substance use disorders, with atypical antipsychotics and several antidepressants acting as antagonists or inverse agonists at 5‑HT2A, and with hallucinogenic psychedelics functioning as high‑efficacy 5‑HT2A agonists that induce characteristic alterations in perception and self‑processing via cortical network reorganization.

Background

SR‑2A corresponds to the serotonin 2A receptor (5‑HT2A/HTR2A), a class A G protein‑coupled receptor that is widely expressed in cortex, limbic regions, platelets, and peripheral tissues, where it transduces serotonergic signals into phospholipase C activation, intracellular calcium mobilization, and downstream changes in neuronal excitability, synaptic plasticity, and smooth muscle tone. The receptor has the canonical seven transmembrane helical bundle with extracellular loops contributing to ligand binding, an orthosteric site that accommodates serotonin and a broad range of psychoactive agonists and antagonists, and an intracellular face that couples primarily to Gq/11 proteins, enabling 5‑HT2A to link monoamine neurotransmission to phosphoinositide hydrolysis and IP3/DAG second messenger generation. Activation of 5‑HT2A stimulates PLCβ, leading to IP3‑dependent Ca²⁺ release and DAG‑mediated PKC activation, and also engages β‑arrestin–dependent scaffolding and multiple kinase pathways, including ERK, which together regulate gene expression, receptor desensitization, and long‑term changes in neuronal circuits involved in mood, perception, and cognition. Central 5‑HT2A receptors are highly expressed on pyramidal neurons in prefrontal cortex and other associative areas, where they modulate glutamatergic output and participate in stress and danger‑related responses; stress exposure and glucocorticoid signaling upregulate cortical 5‑HT2A expression and function, supporting the idea that this receptor constitutes part of a stress‑response system that adjusts cortical processing under threat. Dysregulated 5‑HT2A signaling in major depression, schizophrenia, and substance use disorders, with atypical antipsychotics and several antidepressants acting as antagonists or inverse agonists at 5‑HT2A, and with hallucinogenic psychedelics functioning as high‑efficacy 5‑HT2A agonists that induce characteristic alterations in perception and self‑processing via cortical network reorganization.

References
https://pubmed.ncbi.nlm.nih.gov/26500553/ https://pubmed.ncbi.nlm.nih.gov/21204452/

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%