PARP10

Official Full Name

poly(ADP-ribose) polymerase family member 10

Organism

Homo sapiens

GeneID

84875

Background

Poly(ADP-ribose) polymerases (PARPs), such as PARP10, regulate gene transcription by altering chromatin organization by adding ADP-ribose to histones. PARPs can also function as transcriptional cofactors (Yu et al., 2005 [PubMed 15674325]).[supplied by OMIM, Mar 2008]

Synonyms

ARTD10;

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Detailed Information

PARP10 works as a modulator in mitochondrial function

As a member of the PARP family, which performs mono-ADP-ribosylation of target proteins, poly (ADP-ribose) polymerase (PARP10) was demonstrated to have some linkages with metabolic processes and metabolic regulators, which may give a hint that PARP10 may have influences on mitochondrial oxidative metabolism. In cellular models of breast, cervical, colorectal and exocrine pancreas cancer, specific shRNAs mediated PARP10 knockout can increase mitochondrial oxidative capability. Mitochondrial superoxide production decrease induced by silencing of PARP10 is in accordance with increased expression of antioxidant genes. However, mitochondrial oxidative capacity was found to have a relationship with increased AMPK activation. In MCF7 and CaCo2 cells, silencing of PARP10 can decrease the proliferation rate linked with increased expression of anti-Warburg enzyme. The fact that lower PARP10 expression increases survival in gastric cancer can be analyzed from the online database.

Role of PARP10 in cellular proliferation and tumorigenesis

It is known that the exposition of cells in carcinogenesis to the increased replication stress was the result of the replication fork arrest as sites of DNA lesions and difficulty to replicate genomic regions. Efficient fork restart and DNA repair have a significant role in cancer cell proliferation. Interactions between ADP-ribosyltransferase PARP10 and the replication protein were demonstrated in the previous studies to promote lesion bypass by the recruitment of specialized, non-replicative DNA polymerases. In a large proportion of human tumors, PARP10 was found to be over-expressed. In order to fully reveal the role of PARP10 in cellular transformation, inactivation of PARP10 by CRISPR/Cas9 in Hela cancer cells, and overexpression of it in non-transformed RPE-1 cells were deployed. And it found that cellular proliferation can be promoted by PARP10, whose overexpression has relations with alleviation of cellular sensitivity to replication stress and restart of stalled replication forks. Loss of PARP10 in the xenograft models can reduce the tumorigenesis activity of Hela cells, however, overexpression gives rise to tumor formation by non-transformed RPE-1 cells. PARP10 was indicated to the role as a promoter for cellular transformation through alleviating the replication stress.

Figure 1. A chemical genetics strategy for generating selective inhibitors of PARP10. (Rory K Morgan, et al. 2015)

References:

Morgan R K, Carter-O'Connell I, Cohen M S. Selective inhibition of PARP10 using a chemical genetics strategy. Bioorganic & medicinal chemistry letters, 2015, 25(21): 4770-4773.
Schleicher E M, Galvan A M, Imamura-Kawasawa Y, et al. PARP10 promotes cellular proliferation and tumorigenesis by alleviating replication stress. Nucleic acids research, 2018, 46(17): 8908-8916.
Marton J, Fodor T, Nagy L, et al. PARP10 (ARTD10) modulates mitochondrial function. PLoS One, 2018, 13(1): e0187789.

Quick Inquiry

Interested in learning more?

Contact us today for a free consultation with the scientific team and discover how Creative Biogene can be a valuable resource and partner for your organization.

Request a quote today!

Inquiry