TITLE

mtDNA depletion confers specific gene expression profiles in human cells grown in culture and in xenograft

PUB. DATE
January 2008
SOURCE
BMC Genomics;2008 Supplement 2, Vol. 9, p521
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
No abstract available.
ACCESSION #
43774989

 

Related Articles

  • The regulation of mitochondrial DNA copy number in glioblastoma cells. Dickinson, A; Yeung, K Y; Donoghue, J; Baker, M J; Kelly, R DW; McKenzie, M; Johns, T G; St. John, J C // Cell Death & Differentiation;Dec2013, Vol. 20 Issue 12, p1644 

    As stem cells undergo differentiation, mitochondrial DNA (mtDNA) copy number is strictly regulated in order that specialized cells can generate appropriate levels of adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS) to undertake their specific functions. It is not...

  • Interspecies Somatic Cell Nuclear Transfer Is Dependent on Compatible Mitochondrial DNA and Reprogramming Factors. Yan Jiang; Kelly, Richard; Peters, Amy; Fulka, Helena; Dickinson, Adam; Mitchell, Daniel A.; St. John, Justin C. // PLoS ONE;2011, Vol. 6 Issue 4, p1 

    Interspecies somatic cell nuclear transfer (iSCNT) involves the transfer of a nucleus or cell from one species into the cytoplasm of an enucleated oocyte from another. Once activated, reconstructed oocytes can be cultured in vitro to blastocyst, the final stage of preimplantation development....

  • Mitochondrial DNA stress primes the antiviral innate immune response. West, A. Phillip; Khoury-Hanold, William; Staron, Matthew; Tal, Michal C.; Pineda, Cristiana M.; Lang, Sabine M.; Bestwick, Megan; Duguay, Brett A.; Raimundo, Nuno; MacDuff, Donna A.; Kaech, Susan M.; Smiley, James R.; Means, Robert E.; Iwasaki, Akiko; Shadel, Gerald S. // Nature;4/23/2015, Vol. 520 Issue 7548, p553 

    Mitochondrial DNA (mtDNA) is normally present at thousands of copies per cell and is packaged into several hundred higher-order structures termed nucleoids. The abundant mtDNA-binding protein TFAM (transcription factor A, mitochondrial) regulates nucleoid architecture, abundance and segregation....

  • How Do Human Cells React to the Absence of Mitochondrial DNA? Mineri, Rossana; Pavelka, Norman; Fernandez-Vizarra, Erika; Ricciardi-Castagnoli, Paola; Zeviani, Massimo; Tiranti, Valeria // PLoS ONE;2009, Vol. 4 Issue 5, p1 

    Background: Mitochondrial biogenesis is under the control of two different genetic systems: the nuclear genome (nDNA) and the mitochondrial genome (mtDNA). The mtDNA is a circular genome of 16.6 kb encoding 13 of the approximately 90 subunits that form the respiratory chain, the remaining ones...

  • Prkdc participates in mitochondrial genome maintenance and prevents Adriamycin-induced nephropathy in mice. Papeta, Natalia; Zongyu Zheng; Schon, Eric A.; Brosel, Sonja; Altintas, Mehmet M.; Nasr, Samih H.; Reiser, Jochen; D'Agati, Vivette D.; Gharavi, Ali G.; Zheng, Zongyu // Journal of Clinical Investigation;Nov2010, Vol. 120 Issue 11, p4055 

    Adriamycin (ADR) is a commonly used chemotherapeutic agent that also produces significant tissue damage. Mutations to mitochondrial DNA (mtDNA) and reductions in mtDNA copy number have been identified as contributors to ADR-induced injury. ADR nephropathy only occurs among specific mouse inbred...

  • Clinical, biochemical, cellular and molecular characterization of mitochondrial DNA depletion syndrome due to novel mutations in the MPV17 gene. Uusimaa, Johanna; Evans, Julie; Smith, Conrad; Butterworth, Anna; Craig, Kate; Ashley, Neil; Liao, Chunyan; Carver, Janet; Diot, Alan; Macleod, Lorna; Hargreaves, Iain; Al-Hussaini, Abdulrahman; Faqeih, Eissa; Asery, Ali; Al Balwi, Mohammed; Eyaid, Wafaa; Al-Sunaid, Areej; Kelly, Deirdre; van Mourik, Indra; Ball, Sarah // European Journal of Human Genetics;Feb2014, Vol. 22 Issue 2, p184 

    Mitochondrial DNA (mtDNA) depletion syndromes (MDS) are severe autosomal recessive disorders associated with decreased mtDNA copy number in clinically affected tissues. The hepatocerebral form (mtDNA depletion in liver and brain) has been associated with mutations in the POLG, PEO1 (Twinkle),...

  • Modeling Pathogenic Mutations of Human Twinkle in Drosophila Suggests an Apoptosis Role in Response to Mitochondrial Defects. Sanchez-Martinez, Alvaro; Calleja, Manuel; Peralta, Susana; Matsushima, Yuichi; Hernandez-Sierra, Rosana; Whitworth, Alexander J.; Kaguni, Laurie S.; Garesse, Rafael; Bai, Yidong // PLoS ONE;Aug2012, Vol. 7 Issue 8, Special section p1 

    The human gene C10orf2 encodes the mitochondrial replicative DNA helicase Twinkle, mutations of which are responsible for a significant fraction of cases of autosomal dominant progressive external ophthalmoplegia (adPEO), a human mitochondrial disease caused by defects in intergenomic...

  • Partial Depletion of Mitochondrial DNA from Human Skin Fibroblasts Induces a Gene Expression Profile Reminiscent of Photoaged Skin. Schroeber, Peter; Gremmel, Tobias; Berneburg, Mark; Krutmann, Jean // Journal of Investigative Dermatology;Sep2008, Vol. 128 Issue 9, p2297 

    In photoaged skin, wrinkles result from an increased degradation and a decreased de novo synthesis of collagen fibers. At the molecular level, photoaged skin is characterized by increased amounts of large-scale deletions of the mitochondrial (mt) genome such as the 4,977 bp common deletion. The...

  • Mitochondrial DNA polymerase-γ and human disease. Hudson, Gavin; Chinnery, Patrick F. // Human Molecular Genetics;2006, Vol. 15 Issue suppl_2, pR244 

    The maintenance of mitochondrial DNA (mtDNA) is critically dependent upon polymerase-γ (pol-γ), encoded by the nuclear gene POLG. Over the last 5 years, it has become clear that mutations of POLG are a major cause of human disease. Secondary mtDNA defects characterize these disorders, with...

  • Mitochondrial DNA polymerase-γ and human disease. Hudson, Gavin; Chinnery, Patrick F. // Human Molecular Genetics;Jan2006, Vol. 15 Issue 2, pr244 

    The maintenance of mitochondrial DNA (mtDNA) is critically dependent upon polymerase-γ (pol-γ), encoded by the nuclear gene POLG. Over the last 5 years, it has become clear that mutations of POLG are a major cause of human disease. Secondary mtDNA defects characterize these disorders, with...

Share

Read the Article

Courtesy of THE LIBRARY OF VIRGINIA

Sorry, but this item is not currently available from your library.

Try another library?
Sign out of this library

Other Topics