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Items: 1 to 20 of 138

1.

Insight into the roles of helicase motif Ia by characterizing Fanconi anemia group J protein (FANCJ) patient mutations.

Guo M, Vidhyasagar V, Ding H, Wu Y.

J Biol Chem. 2014 Apr 11;289(15):10551-65. doi: 10.1074/jbc.M113.538892. Epub 2014 Feb 25.

2.

The Q motif of Fanconi anemia group J protein (FANCJ) DNA helicase regulates its dimerization, DNA binding, and DNA repair function.

Wu Y, Sommers JA, Loiland JA, Kitao H, Kuper J, Kisker C, Brosh RM Jr.

J Biol Chem. 2012 Jun 22;287(26):21699-716. doi: 10.1074/jbc.M112.351338. Epub 2012 May 10.

3.

Fanconi anemia group J mutation abolishes its DNA repair function by uncoupling DNA translocation from helicase activity or disruption of protein-DNA complexes.

Wu Y, Sommers JA, Suhasini AN, Leonard T, Deakyne JS, Mazin AV, Shin-Ya K, Kitao H, Brosh RM Jr.

Blood. 2010 Nov 11;116(19):3780-91. doi: 10.1182/blood-2009-11-256016. Epub 2010 Jul 16.

4.

FANCJ helicase uniquely senses oxidative base damage in either strand of duplex DNA and is stimulated by replication protein A to unwind the damaged DNA substrate in a strand-specific manner.

Suhasini AN, Sommers JA, Mason AC, Voloshin ON, Camerini-Otero RD, Wold MS, Brosh RM Jr.

J Biol Chem. 2009 Jul 3;284(27):18458-70. doi: 10.1074/jbc.M109.012229. Epub 2009 May 5.

5.
6.

FANCJ helicase defective in Fanconia anemia and breast cancer unwinds G-quadruplex DNA to defend genomic stability.

Wu Y, Shin-ya K, Brosh RM Jr.

Mol Cell Biol. 2008 Jun;28(12):4116-28. doi: 10.1128/MCB.02210-07. Epub 2008 Apr 21.

7.

FANCJ uses its motor ATPase to destabilize protein-DNA complexes, unwind triplexes, and inhibit RAD51 strand exchange.

Sommers JA, Rawtani N, Gupta R, Bugreev DV, Mazin AV, Cantor SB, Brosh RM Jr.

J Biol Chem. 2009 Mar 20;284(12):7505-17. doi: 10.1074/jbc.M809019200. Epub 2009 Jan 16.

8.

Specialization among iron-sulfur cluster helicases to resolve G-quadruplex DNA structures that threaten genomic stability.

Bharti SK, Sommers JA, George F, Kuper J, Hamon F, Shin-ya K, Teulade-Fichou MP, Kisker C, Brosh RM Jr.

J Biol Chem. 2013 Sep 27;288(39):28217-29. doi: 10.1074/jbc.M113.496463. Epub 2013 Aug 9.

9.

Novel function of the Fanconi anemia group J or RECQ1 helicase to disrupt protein-DNA complexes in a replication protein A-stimulated manner.

Sommers JA, Banerjee T, Hinds T, Wan B, Wold MS, Lei M, Brosh RM Jr.

J Biol Chem. 2014 Jul 18;289(29):19928-41. doi: 10.1074/jbc.M113.542456. Epub 2014 Jun 3.

10.

Interaction between the helicases genetically linked to Fanconi anemia group J and Bloom's syndrome.

Suhasini AN, Rawtani NA, Wu Y, Sommers JA, Sharma S, Mosedale G, North PS, Cantor SB, Hickson ID, Brosh RM Jr.

EMBO J. 2011 Feb 16;30(4):692-705. doi: 10.1038/emboj.2010.362. Epub 2011 Jan 14.

11.

Fanconi anemia group J helicase and MRE11 nuclease interact to facilitate the DNA damage response.

Suhasini AN, Sommers JA, Muniandy PA, Coulombe Y, Cantor SB, Masson JY, Seidman MM, Brosh RM Jr.

Mol Cell Biol. 2013 Jun;33(11):2212-27. doi: 10.1128/MCB.01256-12. Epub 2013 Mar 25.

12.

The FANCJ/MutLalpha interaction is required for correction of the cross-link response in FA-J cells.

Peng M, Litman R, Xie J, Sharma S, Brosh RM Jr, Cantor SB.

EMBO J. 2007 Jul 11;26(13):3238-49. Epub 2007 Jun 21.

13.
14.

The Fanconi anemia proteins FANCD2 and FANCJ interact and regulate each other's chromatin localization.

Chen X, Wilson JB, McChesney P, Williams SA, Kwon Y, Longerich S, Marriott AS, Sung P, Jones NJ, Kupfer GM.

J Biol Chem. 2014 Sep 12;289(37):25774-82. doi: 10.1074/jbc.M114.552570. Epub 2014 Jul 28.

15.

Inhibition of BACH1 (FANCJ) helicase by backbone discontinuity is overcome by increased motor ATPase or length of loading strand.

Gupta R, Sharma S, Doherty KM, Sommers JA, Cantor SB, Brosh RM Jr.

Nucleic Acids Res. 2006;34(22):6673-83. Epub 2006 Dec 1.

16.

Fanconi anemia and Bloom's syndrome crosstalk through FANCJ-BLM helicase interaction.

Suhasini AN, Brosh RM Jr.

Trends Genet. 2012 Jan;28(1):7-13. doi: 10.1016/j.tig.2011.09.003. Epub 2011 Oct 23.

17.

FANCJ localization by mismatch repair is vital to maintain genomic integrity after UV irradiation.

Guillemette S, Branagan A, Peng M, Dhruva A, Schärer OD, Cantor SB.

Cancer Res. 2014 Feb 1;74(3):932-44. doi: 10.1158/0008-5472.CAN-13-2474. Epub 2013 Dec 18.

18.

Mutational analysis of the breast cancer susceptibility gene BRIP1 /BACH1/FANCJ in high-risk non-BRCA1/BRCA2 breast cancer families.

Guénard F, Labrie Y, Ouellette G, Joly Beauparlant C, Simard J, Durocher F; INHERIT BRCAs.

J Hum Genet. 2008;53(7):579-91. doi: 10.1007/s10038-008-0285-z. Epub 2008 Apr 15.

PMID:
18414782
19.

Disease-causing missense mutations in human DNA helicase disorders.

Suhasini AN, Brosh RM Jr.

Mutat Res. 2013 Apr-Jun;752(2):138-52. doi: 10.1016/j.mrrev.2012.12.004. Epub 2012 Dec 28. Review.

20.

Biochemical characterization of Warsaw breakage syndrome helicase.

Wu Y, Sommers JA, Khan I, de Winter JP, Brosh RM Jr.

J Biol Chem. 2012 Jan 6;287(2):1007-21. doi: 10.1074/jbc.M111.276022. Epub 2011 Nov 18.

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