M
Mila E. McCurrach
Researcher at Cold Spring Harbor Laboratory
Publications - 20
Citations - 10282
Mila E. McCurrach is an academic researcher from Cold Spring Harbor Laboratory. The author has contributed to research in topics: Apoptosis & Retinoblastoma protein. The author has an hindex of 17, co-authored 20 publications receiving 9805 citations.
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Journal ArticleDOI
Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a
TL;DR: It is shown that expression of oncogenic ras in primary human or rodent cells results in a permanent G1 arrest, and that the onset of cellular senescence does not simply reflect the accumulation of cell divisions, but can be prematurely activated in response to an onCogenic stimulus.
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FADD: Essential for Embryo Development and Signaling from Some, But Not All, Inducers of Apoptosis
Wen-Chen Yeh,José Luis de la Pompa,Mila E. McCurrach,Hong-Bing Shu,Andrew J. Elia,Arda Shahinian,Michelle Ng,Andrew Wakeham,Wilson Khoo,Kyran O. Mitchell,Wafik S. El-Deiry,Scott W. Lowe,David V. Goeddel,Tak W. Mak +13 more
TL;DR: CD95, tumor necrosis factor receptor type 1 (TNFR-1), and death receptor 3 (DR3) did not induce apoptosis in FADD-deficient embryonic fibroblasts, whereas DR4, oncogenes E1A and c-myc, and chemotherapeutic agent adriamycin did.
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Essential contribution of caspase 3/CPP32 to apoptosis and its associated nuclear changes
Minna Woo,Razqallah Hakem,Maria S. Soengas,Gordon S. Duncan,Arda Shahinian,David Kägi,Anne Hakem,Mila E. McCurrach,Wilson Khoo,Stephen Kaufman,Giorgio Senaldi,Tamara Howard,Scott W. Lowe,Tak W. Mak +13 more
TL;DR: Examination of the role of CPP32 in apoptosis using mice, embryonic stem cells, and mouse embryonic fibroblasts deficient for the caspase indicates that CPP 32 is an essential component in apoptotic events that is remarkably system- and stimulus-dependent.
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E1A signaling to p53 involves the p19(ARF) tumor suppressor.
Elisa de Stanchina,Mila E. McCurrach,Frederique Zindy,Sheau-Yann Shieh,Gerardo Ferbeyre,Andrew V. Samuelson,Carol Prives,Martine F. Roussel,Charles J. Sherr,Scott W. Lowe +9 more
TL;DR: Reintroduction of p19(ARF) functions as part of a p53-dependent failsafe mechanism to counter uncontrolled proliferation and may contribute to E1A's ability to enhance radio- and chemosensitivity.
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INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53
TL;DR: In conclusion, the Emu-myc transgenic lymphoma model generated genetically defined tumors with mutations in the INK4a/ARF, Rb, or p53 genes, which led to aggressive tumors by disrupting overlapping tumor suppressor functions.