PARL Protein, Human (Cell-Free, Myc)

PARL proteins play a critical role in regulating apoptosis during postnatal growth. It is essential for processing the anti-apoptotic form of OPA1, preventing mitochondrial cytochrome c release in response to intrinsic apoptotic signals. PARL Protein, Human (Cell-Free, Myc) is the recombinant human-derived PARL protein, expressed by E. coli Cell-free , with C-Myc labeled tag. The total length of PARL Protein, Human (Cell-Free, Myc) is 327 a.a., with molecular weight of 37.8 kDa.

PARL emerges as a pivotal player in the intricate orchestration of cellular processes, particularly in the control of apoptosis during postnatal growth. Its essential role lies in the proteolytic processing of an antiapoptotic form of OPA1, preventing the release of mitochondrial cytochrome c in response to intrinsic apoptotic signals. Additionally, PARL is indispensable for the maturation of PINK1, facilitating its transformation into the 52kDa mature form after cleavage by mitochondrial-processing peptidase (MPP). Notably, PARL exhibits versatility by mediating the cleavage of serine/threonine-protein phosphatase PGAM5 in damaged mitochondria, responding dynamically to the loss of mitochondrial membrane potential. Moreover, PARL contributes to the processing of CLPB, DIABLO/SMAC, STARD7, and TTC19, unveiling its multifaceted involvement in shaping mitochondrial function and morphology, with implications for apoptotic activity and cellular health.

Human

E. coli Cell-free

C-Myc

Q9H300 (F53-K379)

55486

FRKAPRKVEPRRSDPGTSGEAYKRSALIPPVEETVFYPSPYPIRSLIKPLFFTVGFTGCAFGSAAIWQYESLKSRVQSYFDGIKADWLDSIRPQKEGDFRKEINKWWNNLSDGQRTVTGIIAANVLVFCLWRVPSLQRTMIRYFTSNPASKVLCSPMLLSTFSHFSLFHMAANMYVLWSFSSSIVNILGQEQFMAVYLSAGVISNFVSYVGKVATGRYGPSLGASGAIMTVLAAVCTKIPEGRLAIIFLPMFTFTAGNALKAIIAMDTAGMILGWKFFDHAAHLGGALFGIWYVTYGHELIWKNREPLVKIWHEIRTNGPKKGGGSK

37.8 kDa

Greater than 90% as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.