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Items: 23


A Collaborative Model for Accelerating the Discovery and Translation of Cancer Therapies.

Maertens O, McCurrach ME, Braun BS, De Raedt T, Epstein I, Huang TQ, Lauchle JO, Lee H, Wu J, Cripe TP, Clapp DW, Ratner N, Shannon K, Cichowski K.

Cancer Res. 2017 Nov 1;77(21):5706-5711. doi: 10.1158/0008-5472.CAN-17-1789. Epub 2017 Oct 9. Review.


The atypical E2F family member E2F7 couples the p53 and RB pathways during cellular senescence.

Aksoy O, Chicas A, Zeng T, Zhao Z, McCurrach M, Wang X, Lowe SW.

Genes Dev. 2012 Jul 15;26(14):1546-57. doi: 10.1101/gad.196238.112.


Dissecting the unique role of the retinoblastoma tumor suppressor during cellular senescence.

Chicas A, Wang X, Zhang C, McCurrach M, Zhao Z, Mert O, Dickins RA, Narita M, Zhang M, Lowe SW.

Cancer Cell. 2010 Apr 13;17(4):376-87. doi: 10.1016/j.ccr.2010.01.023.


Mouse models of human AML accurately predict chemotherapy response.

Zuber J, Radtke I, Pardee TS, Zhao Z, Rappaport AR, Luo W, McCurrach ME, Yang MM, Dolan ME, Kogan SC, Downing JR, Lowe SW.

Genes Dev. 2009 Apr 1;23(7):877-89. doi: 10.1101/gad.1771409.


p400 is required for E1A to promote apoptosis.

Samuelson AV, Narita M, Chan HM, Jin J, de Stanchina E, McCurrach ME, Narita M, Fuchs M, Livingston DM, Lowe SW.

J Biol Chem. 2005 Jun 10;280(23):21915-23. Epub 2005 Feb 28.


DNA damage responses and chemosensitivity in the E mu-myc mouse lymphoma model.

Schmitt CA, Wallace-Brodeur RR, Rosenthal CT, McCurrach ME, Lowe SW.

Cold Spring Harb Symp Quant Biol. 2000;65:499-510. No abstract available.


Direct coupling of the cell cycle and cell death machinery by E2F.

Nahle Z, Polakoff J, Davuluri RV, McCurrach ME, Jacobson MD, Narita M, Zhang MQ, Lazebnik Y, Bar-Sagi D, Lowe SW.

Nat Cell Biol. 2002 Nov;4(11):859-64.


Oncogenic properties of PPM1D located within a breast cancer amplification epicenter at 17q23.

Li J, Yang Y, Peng Y, Austin RJ, van Eyndhoven WG, Nguyen KC, Gabriele T, McCurrach ME, Marks JR, Hoey T, Lowe SW, Powers S.

Nat Genet. 2002 Jun;31(2):133-4. Epub 2002 May 20.


Oncogenic ras and p53 cooperate to induce cellular senescence.

Ferbeyre G, de Stanchina E, Lin AW, Querido E, McCurrach ME, Hannon GJ, Lowe SW.

Mol Cell Biol. 2002 May;22(10):3497-508.


Methods for studying pro- and antiapoptotic genes in nonimmortal cells.

McCurrach ME, Lowe SW.

Methods Cell Biol. 2001;66:197-227. No abstract available.


PERP, an apoptosis-associated target of p53, is a novel member of the PMP-22/gas3 family.

Attardi LD, Reczek EE, Cosmas C, Demicco EG, McCurrach ME, Lowe SW, Jacks T.

Genes Dev. 2000 Mar 15;14(6):704-18. Erratum in: Genes Dev 2000 Jul 15;14(14):1835.


INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53.

Schmitt CA, McCurrach ME, de Stanchina E, Wallace-Brodeur RR, Lowe SW.

Genes Dev. 1999 Oct 15;13(20):2670-7.


E1A signaling to p53 involves the p19(ARF) tumor suppressor.

de Stanchina E, McCurrach ME, Zindy F, Shieh SY, Ferbeyre G, Samuelson AV, Prives C, Roussel MF, Sherr CJ, Lowe SW.

Genes Dev. 1998 Aug 1;12(15):2434-42.


Essential contribution of caspase 3/CPP32 to apoptosis and its associated nuclear changes.

Woo M, Hakem R, Soengas MS, Duncan GS, Shahinian A, K├Ągi D, Hakem A, McCurrach M, Khoo W, Kaufman SA, Senaldi G, Howard T, Lowe SW, Mak TW.

Genes Dev. 1998 Mar 15;12(6):806-19.


FADD: essential for embryo development and signaling from some, but not all, inducers of apoptosis.

Yeh WC, de la Pompa JL, McCurrach ME, Shu HB, Elia AJ, Shahinian A, Ng M, Wakeham A, Khoo W, Mitchell K, El-Deiry WS, Lowe SW, Goeddel DV, Mak TW.

Science. 1998 Mar 20;279(5358):1954-8.


Oncogene-dependent apoptosis in extracts from drug-resistant cells.

Fearnhead HO, McCurrach ME, O'Neill J, Zhang K, Lowe SW, Lazebnik YA.

Genes Dev. 1997 May 15;11(10):1266-76.


bax-deficiency promotes drug resistance and oncogenic transformation by attenuating p53-dependent apoptosis.

McCurrach ME, Connor TM, Knudson CM, Korsmeyer SJ, Lowe SW.

Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2345-9.


Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a.

Serrano M, Lin AW, McCurrach ME, Beach D, Lowe SW.

Cell. 1997 Mar 7;88(5):593-602.


Foci of trinucleotide repeat transcripts in nuclei of myotonic dystrophy cells and tissues.

Taneja KL, McCurrach M, Schalling M, Housman D, Singer RH.

J Cell Biol. 1995 Mar;128(6):995-1002.


Genomic organization and transcriptional units at the myotonic dystrophy locus.

Shaw DJ, McCurrach M, Rundle SA, Harley HG, Crow SR, Sohn R, Thirion JP, Hamshere MG, Buckler AJ, Harper PS, et al.

Genomics. 1993 Dec;18(3):673-9.


Molecular basis of myotonic dystrophy: expansion of a trinucleotide (CTG) repeat at the 3' end of a transcript encoding a protein kinase family member.

Brook JD, McCurrach ME, Harley HG, Buckler AJ, Church D, Aburatani H, Hunter K, Stanton VP, Thirion JP, Hudson T, et al.

Cell. 1992 Apr 17;69(2):385. No abstract available.


Molecular basis of myotonic dystrophy: expansion of a trinucleotide (CTG) repeat at the 3' end of a transcript encoding a protein kinase family member.

Brook JD, McCurrach ME, Harley HG, Buckler AJ, Church D, Aburatani H, Hunter K, Stanton VP, Thirion JP, Hudson T, et al.

Cell. 1992 Feb 21;68(4):799-808. Erratum in: Cell. 1992 Apr 17;69(2):385.


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