N
Natalie O. Karpinich
Researcher at University of North Carolina at Chapel Hill
Publications - 19
Citations - 991
Natalie O. Karpinich is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Apoptosis & Adrenomedullin. The author has an hindex of 15, co-authored 18 publications receiving 908 citations. Previous affiliations of Natalie O. Karpinich include Sapienza University of Rome & Thomas Jefferson University.
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Journal ArticleDOI
The course of etoposide-induced apoptosis from damage to DNA and p53 activation to mitochondrial release of cytochrome c.
Natalie O. Karpinich,Marco Tafani,Marco Tafani,Ronald J. Rothman,Matteo Antonio Russo,John L. Farber +5 more
TL;DR: A sequence of biochemical events that mediates the apoptosis induced by etoposide is defined, which proceeds by coupling DNA damage to p53 phosphorylation through the action of DNA-PK and releases cytochrome c and culminates in the death of the cells.
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Regulation of Intracellular pH Mediates Bax Activation in HeLa Cells Treated with Staurosporine or Tumor Necrosis Factor-α
Marco Tafani,Marco Tafani,Joshua A. Cohn,Natalie O. Karpinich,Ronald J. Rothman,Matteo Antonio Russo,John L. Farber +6 more
TL;DR: It is concluded that with either staurosporine or TNF a furosemide-sensitive change in pH i is linked to Bax translocation, cytochrome c release, and cell killing.
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Cytochrome c release upon Fas receptor activation depends on translocation of full-length bid and the induction of the mitochondrial permeability transition.
Marco Tafani,Marco Tafani,Natalie O. Karpinich,Kathryn A. Hurster,John G. Pastorino,Timothy G. Schneider,Matteo Antonio Russo,John L. Farber +7 more
TL;DR: It is concluded that the cleaving of PARP in Fas-mediated apoptosis allowed expression of an energy-dependent cell death program that included the translocation of full-length Bid to the mitochondria with induction of the MPT.
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Decoy receptor CXCR7 modulates adrenomedullin-mediated cardiac and lymphatic vascular development.
Klara R. Klein,Natalie O. Karpinich,Scott T. Espenschied,Helen H. Willcockson,William P. Dunworth,Samantha L. Hoopes,Erich J. Kushner,Victoria L. Bautch,Kathleen M. Caron +8 more
TL;DR: Cxcr7(-/-) mice exhibit gain-of-function cardiac and lymphatic vascular phenotypes that can be reversed upon genetic depletion of adrenomedullin ligand, revealing a previously underappreciated role for decoy receptors as molecular rheostats in controlling the timing and extent of GPCR-mediated cardiac and vascular development.
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Cooperativity between MAPK and PI3K signaling activation is required for glioblastoma pathogenesis
Mark Vitucci,Natalie O. Karpinich,Ryan E. Bash,Andrea M. Werneke,Ralf S. Schmid,Kristen K. White,Robert S. McNeill,Byron Huff,Sophie Wang,Terry Van Dyke,C. Ryan Miller,C. Ryan Miller +11 more
TL;DR: It is suggested that cortical astrocytes can be transformed into GBM and that combined dysregulation of MAPK and PI3K signaling revert G1/S-defective astroCytes to a primitive gene expression state.