Parvalbumin Antibody [J22P8] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Lane 1: Human cerebellum, Lane 2: Mouse cerebellum, Lane 3: Rat cerebellum

Usage Information

Dilution
WB1:1000 IP1:50 IHC1:50 - 1:200 IF1:1600

Application
WB, IP, IHC, IF

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
12 kDa

Positive Control	Human cerebellum; Mouse cerebellum; Rat cerebellum; Mouse brain tissue; Human brain; Rat brain; Human kidney; Human B-cell non-Hodgkin lymphoma; Human parathyroid; Mouse colon; Renca syngeneic tumor; Rat eye; Mouse retina; RPMI 8226 cells
Negative Control	Mouse ovary; SK-MEL-28 cells

Datasheet & SDS

Biological Description

Specificity
Parvalbumin Antibody [J22P8] detects endogenous levels of total Parvalbumin protein.

Clone
J22P8

Synonym(s)
Parvalbumin alpha; Alpha-parvalbumin; Alpha-PV; Pvalb; Pva

Background
Parvalbumin (PV, PVALB) is a small, acidic EF-hand calcium-binding protein highly expressed in fast-twitch skeletal muscle fibers and a specific subset of fast-spiking GABAergic interneurons in the brain, where it functions as a slow Ca2+ buffer that fine-tunes intracellular Ca2+ dynamics to support rapid muscle relaxation and high-frequency neuronal firing. PV is a compact protein comprising three helix-loop-helix EF-hand motifs—an AB domain (inactive due to a shortened DxDxDG loop) and functional high-affinity Ca2+/Mg2+-binding CD and EF domains with canonical 12-residue loops that coordinate Ca2+ via oxygen atoms from Asp, Glu, Asn, and main-chain carbonyls. These domains adopt distinct apo (open) and Ca2+-bound (closed) conformations, with the AB domain shielding the hydrophobic core and modulating CD/EF affinities. PV accelerates the initial decay phase of Ca2+ transients after action potentials without strongly reducing peak amplitude, thus preventing Ca2+ build-up, inhibiting short-term synaptic facilitation, and promoting rapid relaxation in muscle by shuttling Ca2+ from troponin C to the sarcoplasmic reticulum while minimizing twitch fusion during repetitive stimulation. In fast-spiking PV+ interneurons, this buffering supports perisomatic inhibition, gamma oscillations, and network synchrony essential for cognition. PV dysfunction or loss in PV+ neurons leads to circuit hyperexcitability, impaired working memory, and GABAergic deficits implicated in schizophrenia, autism spectrum disorders, Alzheimer’s disease, and epilepsy, while muscle-specific roles connect it to myopathies and malignant hyperthermia susceptibility.

Background

Parvalbumin (PV, PVALB) is a small, acidic EF-hand calcium-binding protein highly expressed in fast-twitch skeletal muscle fibers and a specific subset of fast-spiking GABAergic interneurons in the brain, where it functions as a slow Ca2+ buffer that fine-tunes intracellular Ca2+ dynamics to support rapid muscle relaxation and high-frequency neuronal firing. PV is a compact protein comprising three helix-loop-helix EF-hand motifs—an AB domain (inactive due to a shortened DxDxDG loop) and functional high-affinity Ca2+/Mg2+-binding CD and EF domains with canonical 12-residue loops that coordinate Ca2+ via oxygen atoms from Asp, Glu, Asn, and main-chain carbonyls. These domains adopt distinct apo (open) and Ca2+-bound (closed) conformations, with the AB domain shielding the hydrophobic core and modulating CD/EF affinities. PV accelerates the initial decay phase of Ca2+ transients after action potentials without strongly reducing peak amplitude, thus preventing Ca2+ build-up, inhibiting short-term synaptic facilitation, and promoting rapid relaxation in muscle by shuttling Ca2+ from troponin C to the sarcoplasmic reticulum while minimizing twitch fusion during repetitive stimulation. In fast-spiking PV+ interneurons, this buffering supports perisomatic inhibition, gamma oscillations, and network synchrony essential for cognition. PV dysfunction or loss in PV+ neurons leads to circuit hyperexcitability, impaired working memory, and GABAergic deficits implicated in schizophrenia, autism spectrum disorders, Alzheimer’s disease, and epilepsy, while muscle-specific roles connect it to myopathies and malignant hyperthermia susceptibility.

References
https://pubmed.ncbi.nlm.nih.gov/11069288/ https://pubmed.ncbi.nlm.nih.gov/10548066/

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%