Редактирование: PARL

Presenilins-associated rhomboid-like protein, mitochondrial precursor (EC 3.4.21.105) (Mitochondrial intramembrane cleaving protease PARL) [Contains: P-beta (Pbeta)] [PSARL] [PRO2207]

==Publications==

{{medline-entry
|title=Regulation of skeletal muscle oxidative capacity and insulin signaling by the mitochondrial rhomboid protease [[PARL]].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/20444421
|abstract=Type 2 diabetes mellitus (T2DM) and aging are characterized by insulin resistance and impaired mitochondrial energetics. In lower organisms, remodeling by the protease pcp1 ([[PARL]] ortholog) maintains the function and lifecycle of mitochondria. We examined whether variation in [[PARL]] protein content is associated with mitochondrial abnormalities and insulin resistance. [[PARL]] mRNA and mitochondrial mass were both reduced in elderly subjects and in subjects with T2DM. Muscle knockdown of [[PARL]] in mice resulted in malformed mitochondrial cristae, lower mitochondrial content, decreased PGC1alpha protein levels, and impaired insulin signaling. Suppression of [[PARL]] protein in healthy myotubes lowered mitochondrial mass and insulin-stimulated glycogen synthesis and increased reactive oxygen species production. We propose that lower [[PARL]] expression may contribute to the mitochondrial abnormalities seen in aging and T2DM.
|mesh-terms=* Adolescent
* Adult
* Aged
* Aged, 80 and over
* Aging
* Animals
* Cells, Cultured
* Diabetes Mellitus, Type 2
* Glycogen
* Humans
* Insulin
* Metalloproteases
* Mice
* Mice, Knockout
* Middle Aged
* Mitochondria
* Mitochondrial Proteins
* Muscle, Skeletal
* Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
* Reactive Oxygen Species
* Signal Transduction
* Trans-Activators
* Transcription Factors

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3835349
}}