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Bloom syndrome, RecQ helicase-like

Blm, Bloom syndrome protein, DmBlm
The Bloom syndrome gene product is related to the RecQ subset of DExH box-containing DNA helicases and has both DNA-stimulated ATPase and ATP-dependent DNA helicase activities. Mutations causing Bloom syndrome delete or alter helicase motifs and may disable the 3'-5' helicase activity. The normal protein may act to suppress inappropriate recombination. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, WRN, ACID, V1a, Rad51
Papers on Blm
Knockout mouse production assisted by Blm knockdown.
Shinkai et al., Saitama, Japan. In J Reprod Dev, Dec 2015
It is known that knockdown of the Bloom syndrome gene, BLM, enhances HR-mediated gene targeting efficiencies in various cell lines.
System-wide Analysis of SUMOylation Dynamics in Response to Replication Stress Reveals Novel Small Ubiquitin-like Modified Target Proteins and Acceptor Lysines Relevant for Genome Stability.
Vertegaal et al., Leiden, Netherlands. In Mol Cell Proteomics, May 2015
A large subset of these identified proteins function in one network that consists of interacting replication factors, transcriptional regulators, DNA damage response factors including MDC1, ATR-interacting protein ATRIP, the Bloom syndrome protein and the BLM-binding partner RMI1, the crossover junction endonuclease EME1, BRCA1, and CHAF1A.
Multiple mechanisms limit meiotic crossovers: TOP3α and two BLM homologs antagonize crossovers in parallel to FANCM.
Mercier et al., Versailles, France. In Proc Natl Acad Sci U S A, May 2015
Here we identified Topoisomerase3α (TOP3α) and the RECQ4 helicases--the Arabidopsis slow growth suppressor 1 (Sgs1)/Bloom syndrome protein (BLM) homologs--as major barriers to meiotic CO formation.
Cooperation of Blm and Mus81 in development, fertility, genomic integrity and cancer suppression.
Hakem et al., Toronto, Canada. In Oncogene, May 2015
Mutations of BLM lead to Bloom Syndrome, a rare autosomal recessive disorder characterized by elevated levels of sister chromatid exchanges (SCEs), dwarfism, immunodeficiency, infertility and increased cancer predisposition.
Tailoring heated intraperitoneal mitomycin C for peritoneal metastases originating from colorectal carcinoma: a translational approach to improve survival.
Te Velde et al., Amsterdam, Netherlands. In Br J Cancer, Apr 2015
Bloom syndrome protein (BLM) was further analysed by staining for the corresponding protein with immunohistochemistry (IHC) on both CRC cell lines (n=12) and patient material (n=20).
Blm-s, a BH3-only protein enriched in postmitotic immature neurons, is transcriptionally upregulated by p53 during DNA damage.
Huang et al., Taipei, Taiwan. In Cell Rep, 2014
Using mRNA differential display, we identified a Bcl-2 family gene, Blm-s (Bcl-2-like molecule, short form), enriched in postmitotic neurons of the developing cerebral cortex.
Structural mechanisms of human RecQ helicases WRN and BLM.
Kitano, Ikoma, Japan. In Front Genet, 2013
The RecQ family DNA helicases Werner syndrome protein (WRN) and Bloom syndrome protein (BLM) play a key role in protecting the genome against deleterious changes.
The human RecQ helicases BLM and RECQL4 cooperate to preserve genome stability.
Bohr et al., Baltimore, United States. In Nucleic Acids Res, 2012
BLM and RECQL4 interact physically and functionally in vivo and in vitro.
Complex activities of the human Bloom's syndrome helicase are encoded in a core region comprising the RecA and Zn-binding domains.
Kovács et al., Budapest, Hungary. In Nucleic Acids Res, 2012
The results show that the BLM core consisting of solely the two RecA domains and the ZnBD is capable of performing a multitude of mechanochemical activities utilized in DNA repair.
Polarity and bypass of DNA heterology during branch migration of Holliday junctions by human RAD54, BLM, and RECQ1 proteins.
Mazin et al., Philadelphia, United States. In J Biol Chem, 2012
RAD54 that lacks helicase activity is more efficient in DNA heterology bypass than BLM or REQ1 helicases.
The Werner syndrome protein is distinguished from the Bloom syndrome protein by its capacity to tightly bind diverse DNA structures.
Fry et al., Seattle, United States. In Plos One, 2011
Data show that Bloom syndrome helicase (BLM) formed substantial complexes with only G4 quadruplex DNA while binding only marginally other DNA structures.
Bloom's syndrome and PICH helicases cooperate with topoisomerase IIα in centromere disjunction before anaphase.
Amor-Guéret et al., Orsay, France. In Plos One, 2011
Bloom syndrome protein was required for the correct recruitment to the centromere of active topoisomerase IIalpha, an enzyme specialized in the catenation/decatenation process.
A Blm-Recql5 partnership in replication stress response.
Luo et al., Wenzhou, China. In J Mol Cell Biol, 2011
Here, we review our work based on the genetic knockout studies on Blm and Recql5, two members of the mammalian RecQ helicase family.
Roles of Werner syndrome protein in protection of genome integrity.
Bohr et al., Baltimore, United States. In Dna Repair (amst), 2010
The conserved RecQ family also includes RecQ1, Bloom syndrome protein (BLM), RecQ4, and RecQ5 in humans, as well as Sgs1 in Saccharomyces cerevisiae, Rqh1 in Schizosaccharomyces pombe, and homologs in Caenorhabditis elegans, Xenopus laevis, and Drosophila melanogaster.
Emergence of a DNA-damage response network consisting of Fanconi anaemia and BRCA proteins.
Wang, Baltimore, United States. In Nat Rev Genet, 2007
This network consists of many proteins that maintain genome integrity, including ataxia telangiectasia and Rad3 related protein (ATR), Bloom syndrome protein (BLM), and BRCA1.
Genome-wide phenotype analysis in ES cells by regulated disruption of Bloom's syndrome gene.
Takeda et al., Suita, Japan. In Nature, 2004
Cells deficient in the Bloom's syndrome gene (Blm) show an increased rate of loss of heterozygosity.
Mismatch repair genes identified using genetic screens in Blm-deficient embryonic stem cells.
Bradley et al., Cambridge, United Kingdom. In Nature, 2004
Here we have exploited the high rate of mitotic recombination in Bloom's syndrome protein (Blm)-deficient ES cells to generate a genome-wide library of homozygous mutant cells from heterozygous mutations induced with a revertible gene trap retrovirus.
Enhanced tumor formation in mice heterozygous for Blm mutation.
Groden et al., Cincinnati, United States. In Science, 2002
observations indicate that Blm is a modifier of tumor formation in the mouse and that Blm haploinsufficiency is associated with tumor predisposition
[Functional analysis of yeast homologue gene associated with human DNA helicase causative syndromes].
Miyajima, In Kokuritsu Iyakuhin Shokuhin Eisei Kenkyusho Hokoku, 2001
These are the causative genes for Xeroderma pigmentosum (XPB and XPD), Cockayne syndrome (CSB), diffuse collagen disease (Ku80), alpha-thalassmia (ATR-X), Bloom syndrome (BLM), Werner syndrome (WRN) and Rothmund-Thomson syndrome (RTS).
Sterility of Drosophila with mutations in the Bloom syndrome gene--complementation by Ku70.
Engels et al., Madison, United States. In Science, 2001
The Drosophila Dmblm locus is a homolog of the human Bloom syndrome gene, which encodes a helicase of the RECQ family.
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