Download e-book for iPad: Biochemistry and Genetics of RecQ-Helicases by David B. Lombard

By David B. Lombard

Biochemistry And Genetics of RecQ-Helicases offers a history into the function of helicases generally and RecQ helicases in particular in DNA fix. Helicases- enzymes which holiday down hydrogen bonds among nucleic acid strands in a nucleoside triphosphate-dependent manner-are ubiquitous in biology, partaking in methods as diversified as replication, fix, recombination, transcription, and translation. The RecQ-family helicases are a gaggle of helicases that have very important roles within the upkeep of genomic balance in lots of organisms. In people, mutations in 3 RecQ-family helicases result in illness. This e-book completely examines those helicases. Mutations within the BLM gene result in Bloom syndrome, a illness characterised via a susceptibility to many varieties of melanoma. Mutations within the WRN gene reason Werner syndrome, a disorder which in a few respects resembles untimely getting older. eventually, mutations in a newly characterised RecQ-family member, RECQ4, could lead on to the very infrequent recessive ailment Rothmund-Thomson syndrome, a characterised by way of developmental abnormalities and a few aging-like manifestations. This booklet is meant for any researchers invested in those specific problems, or with a basic curiosity in DNA.

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The subcellular localization of BLM has not been fully characterized. Whereas WRN is concentrated in the nucleolus (99), BLM has recently been shown to reside principally in small nuclear foci (66). One class of nuclear foci are known as PML (promylelocytic leukemia) nuclear bodies (NBs). NBs contain at least 15 different proteins, including the cellular growth suppressor PML (166). The function of NBs is enigmatic, although there is some evidence for their roles in transcription (167), replication (168), apoptosis (169, 170) and response to viral infection (171).

7 Loss of mWRN confers accelerated mortality in the p53 mutant background but do not enhance tumorigenesis in response to an exogenous carcinogen Cancer predisposition is hallmark of WS in humans. mWRNo'o;p53-'- and mWRN"'o;p53°'- mice were bred to determine whether mWRN mutations might accelerate the rapid onset of tumor-related mortality in the p53 mutant (159). While mWRN+'o;p53°'o mice lived on average 149 days, mWRNo'-;p53-'animals had a mean lifespan of 122 days (Figure 9; copyright © ASM, used by permission).

INTRODUCTION Bloom syndrome (BS) is a rare recessive autosomal disorder characterized by genome instability , elevated rates of most types of cancers , immunodeficiency, skin photosensitivity, and hypogonadism (59). The gene defective in BS, BLM, encodes a DNA helicase of the RecQ family (64, 68), which also includes E. coli RecQ, S. cerevisiae Sgs1p, S. pombe Rqhl p, and other members in C. elegans and D. melanogaster (13, 15, 17). Human homologues include WRN, the protein defective in the human premature aging disorder Werner syndrome (WS) (95), and also RECQL, RECQ4 and RECQ5 (134).

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