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PARL encodes a mitochondrial integral membrane protein. Additionally we are shipping PARL Antibodies (45) and many more products for this protein.
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pathogenic PINK1 (show PINK1 Proteins) mutants which are not cleaved by PARL affect PINK1 (show PINK1 Proteins) kinase activity and the ability to induce PARK2 (show PARK2 Proteins)-mediated mitophagy.
Common genetic variants of the PINK1 (show PINK1 Proteins) and PARL genes are unlikely to be involved in schizophrenia.
the frequency of the haplotype AAC, and AAT were significantly higher in the unaffected cases and the frequencies of haplotype GGT were significantly higher in LHON cases
Rhomboid protease PARL mediates the mitochondrial membrane potential loss-induced cleavage of PGAM5 (show PGAM5 Proteins).
p.S77N variant, and, possibly, mutations in the PARL protein overall, are not a frequent cause of autosomal recessive early-onset Parkinson's disease
work provides unexpected insights into the structural determinants regulating Parl stability and activity in vivo, and reveals a complex cascade of proteolytic events controlling the function of the protease in the mitochondrion
PARL deficiency impairs PARKIN (show PARK2 Proteins) recruitment to mitochondria.
the PARL-catalyzed removal of the Pink1 (show PINK1 Proteins) signal sequence in the canonical import pathway acts as a cellular checkpoint for mitochondrial integrity
Mitochondrial protease PARL cleaves PINK1 (show PINK1 Proteins) at position A103.
Data show that no association between PARL gene SNPs and LHON in Chinese patients with m.11778G>A.
Downregulation of PARL after ischemia is a key step in ischemic neuronal injury, and that it decreases HtrA2 (show HTRA2 Proteins) processing and increases neuronal vulnerability.
the OPA1/PARL dependent pathway of cristae remodeling is implicated in heat shock.
Suppression of PARL protein in healthy myotubes lowered mitochondrial mass and insulin (show INS Proteins)-stimulated glycogen (show GYS1 Proteins) synthesis and increased reactive oxygen species production.
results indicate a different function and mechanism of Hax1 (show HAX1 Proteins) in apoptosis and re-opens the question of whether mammalian PARL, in addition to apoptosis, regulates mitochondrial stress response through Omi/HtrA2 (show HTRA2 Proteins) processing.
Parl-/- mitochondria display reduced levels of OPA1, and OPA1 specifically targeted to IMS complements Parl-/- cells, substantiating the importance of PARL in OPA1 processing.(PARL protein, mouse)
Hax1 (show HAX1 Proteins), is required to suppress apoptosis in lymphocytes and neurons; suppression requires the interaction of Hax1 (show HAX1 Proteins) with the mitochondrial proteases Parl and HtrA2 (show HTRA2 Proteins)
This gene encodes a mitochondrial integral membrane protein. Following proteolytic processing of this protein, a small peptide (P-beta) is formed and translocated to the nucleus. This gene may be involved in signal transduction via regulated intramembrane proteolysis of membrane-tethered precursor proteins. Variation in this gene has been associated with increased risk for type 2 diabetes. Alternative splicing results in multiple transcript variants encoding different isoforms.
mitochondrial intramembrane cleaving protease PARL
, mitochondrial intramembrane-cleaving protease PARL
, presenilins-associated rhomboid-like protein, mitochondrial
, rhomboid 7 homolog 1
, presenilin associated, rhomboid-like isoform 1 preproprotein
, presenilin associated, rhomboid-like preproprotein