Abstract
DHH superfamily proteins play pivotal roles in various cellular processes like replication, recombination, repair and nucleic acids metabolism. These proteins are important for homeostasis maintenance and stress tolerance in prokaryotes and eukaryotes. The prominent members of DHH superfamily include single-strand specific exonuclease RecJ, nanoRNases, polyphosphatase PPX1, pyrophosphatase, prune phosphodiesterase and cell cycle protein Cdc45. The mutations of genes coding for DHH superfamily proteins lead to severe growth defects and in some cases, may be lethal. The members of superfamily have a wide substrate spectrum. The spectrum of substrate for DHH superfamily members ranges from smaller molecules like pyrophosphate and cyclic nucleotides to longer single-stranded DNA molecule. Several genetic, structural and biochemical studies have provided interesting insights about roles of DHH superfamily members. However, there are still various unexplored members in both prokaryotes and eukaryotes. Many aspects of this superfamily associated with homeostasis maintenance and stress tolerance are still not clearly understood. A comprehensive understanding is pre-requisite to decipher the physiological significance of members of DHH superfamily. This article provides the current understanding of DHH superfamily members and their significance in nucleic acids metabolism and stress tolerance across diverse forms of life.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: International journal of biological macromolecules
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.