Zobrazeno 1 - 10
of 55
pro vyhledávání: '"Hindupur K. Anandatheerthavarada"'
Autor:
Naresh Babu V. Sepuri, Narayan G. Avadhani, Carolyn K. Suzuki, Joseph F. Spear, Manti Guha, Bin Lu, Satish Srinivasan, Rajesh Angireddy, Hindupur K. Anandatheerthavarada
The mitochondrial ATP dependent matrix protease, Lon, is involved in the maintenance of mitochondrial DNA nucleoids and degradation of abnormal or misfolded proteins. The Lon protease regulates mitochondrial Tfam (mitochondrial transcription factor A
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3a07724bd6266422c6f921523b673397
https://europepmc.org/articles/PMC5507603/
https://europepmc.org/articles/PMC5507603/
Autor:
Hindupur K. Anandatheerthavarada, F. Peter Guengerich, Anindya Roy Chowdhury, Seema Bansal, Frank J. Gonzalez, Adrian N. Leu, Narayan G. Avadhani
Publikováno v:
Journal of Biological Chemistry. 289:9936-9951
We report that polycyclic aromatic hydrocarbon (PAH)-inducible CYP1B1 is targeted to mitochondria by sequence-specific cleavage at the N terminus by a cytosolic Ser protease (polyserase 1) to activate the cryptic internal signal. Site-directed mutage
Autor:
F. Peter Guengerich, Narayan G. Avadhani, Martha V. Martin, Hindupur K. Anandatheerthavarada, Michelle C Sangar
Publikováno v:
Molecular Genetics and Metabolism. 99:90-97
Human cytochrome P450 2D6 (CYP2D6) is responsible for the metabolism of approximately 20% of drugs in common clinical use. The CYP2D6 gene locus is highly polymorphic. Many of the polymorphisms have been shown to be clinically relevant and can accoun
Publikováno v:
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1802:11-19
Mitochondrial dysfunction is an important intracellular lesion associated with a wide variety of diseases including neurodegenerative disorders. In addition to aging, oxidative stress and mitochondrial DNA mutations, recent studies have implicated a
Autor:
F. Peter Guengerich, Subbuswamy K. Prabu, Michelle C Sangar, Weigang Tang, Miroslav Dostálek, Martha V. Martin, Hindupur K. Anandatheerthavarada, Narayan G. Avadhani
Publikováno v:
FEBS Journal. 276:3440-3453
Constitutively expressed human cytochrome P450 2D6 (CYP2D6; EC 1.14.14.1) is responsible for the metabolism of approximately 25% of drugs in common clinical use. It is widely accepted that CYP2D6 is localized in the endoplasmic reticulum of cells; ho
Publikováno v:
Journal of Biological Chemistry. 284:17352-17363
Previously we showed that xenobiotic inducible cytochrome P450 (CYP) proteins are bimodally targeted to the endoplasmic reticulum and mitochondria. In this study, we investigated the mechanism of delivery of chimeric signal containing CYP proteins to
Publikováno v:
Proceedings of the National Academy of Sciences. 105:186-191
The environmental toxin 2,3,7,8-tetrachlorodibenzodioxin (TCDD) is a known human carcinogen; however, its precise mechanism of action remains unclear. Here we show that TCDD induces mitochondrial dysfunction, stress signaling, and tumor invasion by a
Publikováno v:
FEBS Journal. 274:4615-4630
Previously we showed that intact rat cytochrome P450 2E1, cytochrome P450 2B1 and truncated cytochrome P450 1A1 are targeted to mitochondria in rat tissues and COS cells. However, some reports suggest that truncated cytochrome P450 2E1 is targeted to
Autor:
Narayan G. Avadhani, Haider Raza, Ji-Kang Fang, Naresh Babu V. Sepuri, Joseph F. Spear, Hindupur K. Anandatheerthavarada, Subbuswamy K. Prabu, Domenico F. Galati
Publikováno v:
FEBS Letters. 581:1302-1310
We have mapped the sites of ischemia/reperfusion-induced phosphorylation of cytochrome c oxidase (CcO) subunits in rabbit hearts by using a combination of Blue Native gel/Tricine gel electrophoresis and nano-LC–MS/MS approaches. We used precursor i
Autor:
Hindupur K. Anandatheerthavarada, Domenico F. Galati, Latha Devi, Badanavalu M. Prabhu, Narayan G. Avadhani
Publikováno v:
The Journal of Neuroscience. 26:9057-9068
Mitochondrial dysfunction is one of the major intracellular lesions of Alzheimer’s disease (AD). However, the causative factors involved in the mitochondrial dysfunction in human AD are not well understood. Here we report that nonglycosylated full-