Literature DB >> 11173860

BLM, the Bloom's syndrome protein, varies during the cell cycle in its amount, distribution, and co-localization with other nuclear proteins.

M M Sanz1, M Proytcheva, N A Ellis, W K Holloman, J German.   

Abstract

BLM, the protein encoded by the gene mutated in Bloom's syndrome (BS), is a phylogenetically highly conserved DNA helicase that varies in amount and distribution in the nucleus during the cell-division cycle. It is undetectable in many cells as they emerge from mitosis but becomes abundant during G(1) and remains so throughout S, G(2), and mitosis. BLM is widely distributed throughout the nucleus but at certain times also becomes concentrated in foci that vary in number and size. It co-localizes transitorily with replication protein A (RPA) and promyelocytic leukemia protein (PML) nuclear bodies, and at times it enters the nucleolus. The observations support the hypothesis that BLM is distributed variously about the nucleus to manipulate DNA in some, very possibly several, nucleic acid transactions, when and where they take place. The specific transaction(s) remain to be identified. Although absence from the nucleus of functional BLM - the situation in BS - obviously is not lethal in the human, other helicases would appear to be unable to substitute for it completely, witness the hypermutability and hyperrecombinability of BS cells. Copyright 2001 S. Karger AG, Basel

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Year:  2000        PMID: 11173860     DOI: 10.1159/000056848

Source DB:  PubMed          Journal:  Cytogenet Cell Genet        ISSN: 0301-0171


  25 in total

1.  The Bloom's syndrome helicase stimulates the activity of human topoisomerase IIIalpha.

Authors:  Leonard Wu; Ian D Hickson
Journal:  Nucleic Acids Res       Date:  2002-11-15       Impact factor: 16.971

2.  NO66, a highly conserved dual location protein in the nucleolus and in a special type of synchronously replicating chromatin.

Authors:  Jens Eilbracht; Michaela Reichenzeller; Michaela Hergt; Martina Schnölzer; Hans Heid; Michael Stöhr; Werner W Franke; Marion S Schmidt-Zachmann
Journal:  Mol Biol Cell       Date:  2004-01-23       Impact factor: 4.138

3.  G4 DNA unwinding by BLM and Sgs1p: substrate specificity and substrate-specific inhibition.

Authors:  Michael D Huber; Damian C Lee; Nancy Maizels
Journal:  Nucleic Acids Res       Date:  2002-09-15       Impact factor: 16.971

Review 4.  RecQ helicases; at the crossroad of genome replication, repair, and recombination.

Authors:  Sarallah Rezazadeh
Journal:  Mol Biol Rep       Date:  2011-09-23       Impact factor: 2.316

5.  Redundancy of DNA helicases in p53-mediated apoptosis.

Authors:  E A Spillare; X W Wang; C von Kobbe; V A Bohr; I D Hickson; C C Harris
Journal:  Oncogene       Date:  2006-03-30       Impact factor: 9.867

6.  Chromosome breakage is regulated by the interaction of the BLM helicase and topoisomerase IIalpha.

Authors:  Beatriz Russell; Saumitri Bhattacharyya; Jeremy Keirsey; April Sandy; Patrick Grierson; Erin Perchiniak; Juraj Kavecansky; Samir Acharya; Joanna Groden
Journal:  Cancer Res       Date:  2011-01-11       Impact factor: 12.701

Review 7.  The BLM dissolvasome in DNA replication and repair.

Authors:  Kelly A Manthei; James L Keck
Journal:  Cell Mol Life Sci       Date:  2013-03-31       Impact factor: 9.261

Review 8.  The role of RecQ helicases in non-homologous end-joining.

Authors:  Guido Keijzers; Scott Maynard; Raghavendra A Shamanna; Lene Juel Rasmussen; Deborah L Croteau; Vilhelm A Bohr
Journal:  Crit Rev Biochem Mol Biol       Date:  2014-07-22       Impact factor: 8.250

9.  DNA end resection is needed for the repair of complex lesions in G1-phase human cells.

Authors:  Nicole B Averbeck; Oliver Ringel; Maren Herrlitz; Burkhard Jakob; Marco Durante; Gisela Taucher-Scholz
Journal:  Cell Cycle       Date:  2014       Impact factor: 4.534

10.  Time to bloom.

Authors:  Shweta Tikoo; Sagar Sengupta
Journal:  Genome Integr       Date:  2010-11-04
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