PARL antibody (Middle Region)

Catalog No. ABIN7879543

The Rabbit Polyclonal anti-PARL antibody (ABIN7879543) specifically detects PARL in WB and FACS. The antibody is reactive with Human, Mouse and Rat samples.

Quick Overview for PARL antibody (Middle Region) (ABIN7879543)

Target: PARL (Presenilin Associated, Rhomboid-Like (PARL))

Reactivity: Human, Mouse, Rat

Host: Rabbit

Clonality: Polyclonal

Conjugate: This PARL antibody is un-conjugated

Application: Western Blotting (WB), Flow Cytometry (FACS)

Product Details anti-PARL Antibody

Binding Specificity: Middle Region

Purpose: PARL Antibody / Presenilins-associated rhomboid-like protein

Purification: Immunogen affinity purified

Immunogen: A synthetic peptide corresponding to a sequence in the middle region of human PARL was used as the immunogen for the PARL antibody.

Isotype: IgG

Application Details

Application Notes: Optimal dilution of the PARL antibody should be determined by the researcher.

Restrictions: For Research Use only

Handling

Format: Lyophilized

Reconstitution: Adding 0.2 mL of distilled water will yield a concentration of 500 μg/mL

Buffer: Each vial contains 4 mg Trehalose, 0.9 mg NaCl, 0.2 mg Na2HPO4.

Storage: 4 °C,-20 °C

Storage Comment: After reconstitution, the PARL antibody can be stored for up to one month at 4oC. For long-term, aliquot and store at -20oC. Avoid repeated freezing and thawing.

Target Details for PARL

Target: PARL (Presenilin Associated, Rhomboid-Like (PARL))

Alternative Name: PARL

Background: PARL antibody detects Presenilins-associated rhomboid-like protein, a mitochondrial intramembrane protease involved in regulating mitochondrial dynamics, apoptosis, and mitophagy. The UniProt recommended name is Presenilins-associated rhomboid-like protein (PARL). This serine protease participates in the regulated intramembrane proteolysis of substrates that control mitochondrial morphology and quality control.

Functionally, PARL antibody identifies a 379-amino-acid protein localized to the inner mitochondrial membrane. PARL cleaves and activates key mitochondrial substrates such as PINK1 and PGAM5, initiating mitophagy and apoptosis signaling pathways. Through these actions, PARL maintains mitochondrial homeostasis and protects cells from oxidative stress. It also participates in remodeling the inner membrane during stress conditions, influencing cristae organization and mitochondrial fission-fusion balance.

The PARL gene is located on chromosome 3q27.1 and is expressed in metabolically active tissues including brain, heart, and skeletal muscle. Expression levels fluctuate with energy demand and stress, with upregulation observed during mitochondrial biogenesis and differentiation. PARL is evolutionarily conserved across eukaryotes, emphasizing its fundamental role in organelle maintenance.

Pathologically, mutations in PARL have been associated with mitochondrial dysfunction, Parkinson's disease, and metabolic disorders. Impaired PARL activity disrupts PINK1 processing, leading to defective mitophagy and accumulation of damaged mitochondria. In contrast, overexpression may alter apoptotic sensitivity by influencing cytochrome c release. Research using PARL antibody supports studies in mitochondrial biology, apoptosis regulation, and neurodegenerative disease.

PARL antibody can be validated for western blotting, immunofluorescence, and immunohistochemistry to detect mitochondrial proteases. NSJ Bioreagents provides PARL antibody reagents optimized for research in mitophagy, proteolytic signaling, and mitochondrial quality control.

Structurally, Presenilins-associated rhomboid-like protein contains seven transmembrane domains forming a proteolytic chamber within the inner mitochondrial membrane. Its catalytic serine and histidine residues form the rhomboid protease active site. The protein's C-terminal region undergoes regulated processing, modulating its activity in stress conditions. This antibody enables investigation of PARL's role in mitochondrial proteostasis and apoptosis signaling.

UniProt: Q9H300

Pathways: Autophagy