Saege Hancock - Concepedia

Author

Saege Hancock

University of Pennsylvania

Also Known As

S. Hancock, Saege A. Hancock, Saege Hancock

Publications

930

Citations

H-Index

Concepts

All Affiliations

University of Pennsylvania Centre Hospitalier Universitaire d'Angers Children's Hospital of Philadelphia Université d'Angers National Institutes of Health

About

Saege Hancock is an author at University of Pennsylvania specializing in medicine, neurodegenerative diseases, and neuroscience.

Top Concepts

#	Concept	H-Index	Publications	Citations
1	Medicine	3	3	257
2	Health Sciences	1	1	45
3	Cellular Physiology	1	1	45
4	Molecular Biology	1	1	113
5	Molecular Genetics	1	1	113

Saege Hancock

Publications

892

Citations

H-Index

Page 1

	Year	Citations
Progressive increase in mtDNA 3243A>G heteroplasmy causes abrupt transcriptional reprogramming Martin Picard, Jiangwen Zhang, Saege Hancock, Proceedings of the National Academy of Sciences	2014	296
Essential role of mitochondrial energy metabolism in Foxp3 <sup>+</sup> T‐regulatory cell function and allograft survival Ulf H. Beier, Alessia Angelin, Tatiana Akimova, The FASEB Journal	2015	260
Mutations of Human NARS2, Encoding the Mitochondrial Asparaginyl-tRNA Synthetase, Cause Nonsyndromic Deafness and Leigh Syndrome Mariella Simon, Élodie M. Richard, Xinjian Wang, PLoS Genetics Neurodegenerative DiseasesMendelian DisorderMitochondrial BiogenesisMitochondrial FunctionGenetic Disorder	2015	113
A novel NDUFA1 mutation leads to a progressive mitochondrial complex I-specific neurodegenerative disease Prasanth Potluri, Antonio Dávila, Eduardo Ruiz‐Pesini, Molecular Genetics and Metabolism Neurodegenerative DiseasesAlzheimer's DiseaseMitochondrial FunctionDegenerative DiseaseDegenerative Pathology	2009	99
Mutation-Enrichment Next-Generation Sequencing for Quantitative Detection of <i>KRAS</i> Mutations in Urine Cell-Free DNA from Patients with Advanced Cancers Takeo Fujii, Afsaneh Barzi, Andrea Sartore‐Bianchi, Clinical Cancer Research	2017	55
Metabolically induced heteroplasmy shifting and l-arginine treatment reduce the energetic defect in a neuronal-like model of MELAS Valérie Desquiret‐Dumas, Naïg Guéguen, Magalie Barth, Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease L-arginine TreatmentEnergetic DefectNeuronal-like ModelMedicinePhysiology	2012	45
DIFFERENTIAL NF-??B AND I??B GENE EXPRESSION DURING DEVELOPMENT OF CARDIAC ALLOGRAFT REJECTION VERSUS CD154 MONOCLONAL ANTIBODY-INDUCED TOLERANCE1 Vilmos Csizmadia, Wei Gao, Saege Hancock, Transplantation	2001	24

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