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Maria S. Soengas

Researcher at University of Michigan

Publications -  73
Citations -  16165

Maria S. Soengas is an academic researcher from University of Michigan. The author has contributed to research in topics: Melanoma & Apoptosis. The author has an hindex of 34, co-authored 70 publications receiving 14407 citations. Previous affiliations of Maria S. Soengas include Carlos III Health Institute & Cold Spring Harbor Laboratory.

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Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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BRAFE600-associated senescence-like cell cycle arrest of human naevi

Chrysiis Michaloglou, +9 more
- 04 Aug 2005 - 
TL;DR: It is shown that sustained BRAFV600E expression in human melanocytes induces cell cycle arrest, which is accompanied by the induction of both p16INK4a and senescence-associated acidic β-galactosidase (SA-β-Gal) activity, a commonly usedsenescence marker.
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Differential requirement for caspase 9 in apoptotic pathways in vivo

Razqallah Hakem, +27 more
- 07 Aug 1998 - 
TL;DR: Comparison of the requirement for Casp9 and Casp3 in different apoptotic settings indicates the existence of at least four different apoptosis pathways in mammalian cells.
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Inactivation of the apoptosis effector Apaf-1 in malignant melanoma.

Maria S. Soengas, +11 more
- 11 Jan 2001 - 
TL;DR: It is concluded that Apaf-1 is inactivated in metastatic melanomas, which leads to defects in the execution of apoptotic cell death, which may contribute to the low frequency of p53 mutations observed in this highly chemoresistant tumour type.
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Mechanisms of apoptosis sensitivity and resistance to the BH3 mimetic ABT-737 in acute myeloid leukemia

Marina Konopleva, +26 more
- 01 Nov 2006 - 
TL;DR: ABT-737 effectively kills acute myeloid leukemia blast, progenitor, and stem cells without affecting normal hematopoietic cells, suggesting that ABT- 737 could be a highly effective antileukemia agent when the mechanisms of resistance identified here are considered.