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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Inhibin, alpha

This gene encodes the alpha subunit of inhibins A and B protein complexes. These complexes negatively regulate follicle stimulating hormone secretion from the pituitary gland. Inhibins have also been implicated in regulating numerous cellular processes including cell proliferation, apoptosis, immune response and hormone secretion.[provided by RefSeq, Dec 2010] (from NCBI)
Top mentioned proteins: ACID, HAD, CAN, OUT, catalase
Papers on InhA
Structural Basis for Latency and Function of Immune Inhibitor A Metallopeptidase, a Modulator of the Bacillus anthracis Secretome.
Gomis-Rüth et al., Barcelona, Spain. In Structure, Feb 2016
Immune inhibitor A(InhA)-type metallopeptidases are potential virulence factors secreted by members of the Bacillus cereus group.
Feeding Anthrax: The Crystal Structure of Bacillus anthracis InhA Protease.
Baumann et al., Köln, Germany. In Structure, Feb 2016
(2016) describe the structural basis of activation and latency of InhA, a major secreted protease of Bacillus anthracis.
Targeting Mycobacterial Enzymes with Natural Products.
Sieniawska, Lublin, Poland. In Chem Biol, Nov 2015
Here, natural metabolites are presented as being inhibitors/activators of the mycobacterial enzymes involved in mycobacterial growth in vitro (ClpC1, ClpP, MurE ligase, mycothiol S-conjugate amidase, β-ketoacyl-ACP synthase, InhA) and in vivo, as regards the host cell (PtpB).
A review of the use of ethionamide and prothionamide in childhood tuberculosis.
Schaaf et al., Cape Town, South Africa. In Tuberculosis (edinb), Nov 2015
ETH and PTH are pro-drugs that, following enzymatic activation by mycobacterial EthA inhibit InhA, a target shared with isoniazid (INH), and subsequently inhibit mycolic acid synthesis of Mycobacterium tuberculosis.
Genetic mutations associated with isoniazid resistance in Mycobacterium tuberculosis: a systematic review.
Rodwell et al., San Diego, United States. In Plos One, 2014
The second most frequently observed mutation, inhA-15, was reported among 19% of phenotypically resistant isolates.
Computational approach to understanding the mechanism of action of isoniazid, an anti-TB drug.
Harinath et al., India. In Int J Mycobacteriol, 2014
This INH intermediate in the presence of NADH forms INH-NAD adduct which inhibits inhA (2-trans-enoyl-acyl carrier protein reductase) of MTB, thus blocking the synthesis of mycolic acid, a major lipid of the mycobacterial cell wall.
Gene variation and premature ovarian failure: a meta-analysis.
Wu et al., Nanjing, China. In Eur J Obstet Gynecol Reprod Biol, 2014
Five genes were selected for analysis, including 10 common gene polymorphisms [BMP15 (-9C>G, 788insTCT and 852C>T), ESR1 (-351A>G and -397C>T), FMR1 CGG repeat, FSHR (919A>G and 2039A>G), INHA (-16C>T and -124A>G)] and two mutations (BMP15 538G>A and INHA 769G>A).
Resistance to Isoniazid and Ethionamide in Mycobacterium tuberculosis: Genes, Mutations, and Causalities.
Jacobs et al., In Microbiol Spectr, 2014
The resulting active species reacts with NAD+ to form an INH-NAD or ETH-NAD adduct, which inhibits the enoyl ACP reductase InhA, leading to mycolic acid biosynthesis inhibition and mycobacterial cell death.
Use of rapid molecular test for multidrug-resistant tuberculosis detection among relapse cases in Cote d'Ivoire.
Dosso et al., Abidjan, Ivory Coast. In Int J Mycobacteriol, 2014
Thirteen mutations conferring a resistance to Isoniazid were observed of which 9 in katG gene and 4 in katG and promoter region of inhA gene.
Drug resistance-related mutations in multidrug-resistant Mycobacterium tuberculosis isolates from diverse geographical regions.
Hoffner et al., Tegucigalpa, Honduras. In Int J Mycobacteriol, 2012
METHODS: In order to analyse the geographical distribution and frequency of mutations conferring resistance to rifampicin, isoniazid and fluoroquinolones, the researchers investigated the presence of mutations in the rpoB gene, the katG gene, the mabA-inhA promoter region and the gyrA gene in clinical isolates of multidrug-resistant tuberculosis (MDR-TB) from Belarus, China, Iran/Iraq, Honduras, Romania and Uganda.
Transcriptional silencing of the inhibin-α gene in human gastric carcinoma cells.
Cho et al., Seoul, South Korea. In Int J Oncol, 2012
the inhibinalpha gene is transcriptionally silenced in human gastric cancer cells
Expression of inhibin/activin proteins and receptors in the human hypothalamus and basal forebrain.
Stopa et al., Providence, United States. In J Neuroendocrinol, 2012
Inhibin alpha subunit staining is not detected in any of the major anatomical regions of the human brain.
Inhibin α-subunit N terminus interacts with activin type IB receptor to disrupt activin signaling.
Woodruff et al., Chicago, United States. In J Biol Chem, 2012
Inhibin alpha-subunit N terminus interacts with activin type IB receptor to disrupt activin signaling.
Expression of transcription factors controlling alpha inhibin gene expression in placental tissues from pregnancies affected by fetal Down syndrome.
Gundogan et al., In Prenat Diagn, 2012
Expression of transcription factors controlling alpha inhibin gene expression in placental tissues from pregnancies affected by fetal Down syndrome.
Immunohistochemical evaluation of inhibin-alpha in non-small-cell lung carcinomas--a pitfall in diagnosing metastatic pulmonary carcinomas.
Lin et al., United States. In Ann Clin Lab Sci, 2011
A subset of primary mixed or acinar and mucin-producing acinar carcinomas (10%) and large-cell carcinomas (22%) expressed inhibin-alpha.
Inhibitors of FabI, an enzyme drug target in the bacterial fatty acid biosynthesis pathway.
Tonge et al., Stony Brook, United States. In Acc Chem Res, 2008
Using structure-based approaches, we have developed a series of alkyl diphenyl ethers that are nanomolar inhibitors of InhA, the FabI from M. tuberculosis, and that are active against INH-resistant strains of M. tuberculosis.
Transfer of a point mutation in Mycobacterium tuberculosis inhA resolves the target of isoniazid.
Jacobs et al., New York City, United States. In Nat Med, 2006
Using specialized linkage transduction, a single point mutation allele (S94A) within the putative target gene inhA was transferred in Mycobacterium tuberculosis.
GroEL1: a dedicated chaperone involved in mycolic acid biosynthesis during biofilm formation in mycobacteria.
Hatfull et al., Pittsburgh, United States. In Cell, 2006
Biofilm formation is associated with elevated synthesis of short-chain (C56-C68) fatty acids, and strains with altered mycolate profiles--including an InhA mutant resistant to the antituberculosis drug isoniazid and a strain overexpressing KasA--are defective in biofilm formation.
Modification of the NADH of the isoniazid target (InhA) from Mycobacterium tuberculosis.
Sacchettini et al., College Station, United States. In Science, 1998
The preferred antitubercular drug isoniazid specifically targets a long-chain enoyl-acyl carrier protein reductase (InhA), an enzyme essential for mycolic acid biosynthesis in Mycobacterium tuberculosis.
Molecular mechanisms of drug resistance in Mycobacterium tuberculosis.
Blanchard, New York City, United States. In Annu Rev Biochem, 1995
Resistance to isoniazid can be caused either by mutations in the katG-encoded catalase-peroxidase, the enzyme responsible for drug activation, or by the molecular target, the inhA-encoded long chain enoyl-ACP reductase.
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