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ATG9 autophagy related 9 homolog B

This gene functions in the regulation of autophagy, a lysosomal degradation pathway. This gene also functions as the antisense to and in the posttranscriptional regulation of endothelial nitric oxide synthase 3. Mutations in this gene and disruption of the autophagy process have been associated with multiple cancers. Transcript evidence indicates this is a nonsense-mediated decay (NMD) candidate; however, published reports support a valid protein. [provided by RefSeq, Oct 2011] (from NCBI)
Top mentioned proteins: CAN, ACID, V1a, Nitric Oxide Synthase, fibrillin-1
Papers on Sone
Anti-hypertensive effect of Lycium barbarum L. with down-regulated expression of renal endothelial lncRNA sONE in a rat model of salt-sensitive hypertension.
Hui et al., Beijing, China. In Int J Clin Exp Pathol, 2014
The present study aims to test whether Lycium barbarum L. has anti-hypertensive effect through regulating expression of lncRNA sONE in a rat model of salt-sensitive hypertension.
Regulation of autophagic activation by Rta of Epstein-Barr virus via the extracellular signal-regulated kinase pathway.
Liu et al., T'ai-chung-shih, Taiwan. In J Virol, 2014
The expression of Rta also activates the transcription of the genes that participate in the formation of autophagosomes, including LC3A, LC3B, and ATG9B genes, as well as those that are involved in the regulation of autophagy, including the genes TNF, IRGM, and TRAIL.
Active stabilization of human endothelial nitric oxide synthase mRNA by hnRNP E1 protects against antisense RNA and microRNAs.
Marsden et al., Toronto, Canada. In Mol Cell Biol, 2013
Significantly, these stabilizing RNP complexes protect eNOS mRNA from the inhibitory effects of its antisense transcript sONE and 3'-UTR-targeting small interfering RNAs (siRNAs), as well as microRNAs, specifically, hsa-miR-765, which targets eNOS mRNA stability determinants.
Construction and analysis of the protein-protein interaction network related to essential hypertension.
Li et al., Ürümqi, China. In Bmc Syst Biol, 2012
Finally, the robustness of NOS3 as central protein and accuracy of backbone were validated by 287 test networks.
NOS3 894G>T polymorphism is associated with progression of kidney disease and cardiovascular morbidity in type 2 diabetic patients: NOS3 as a modifier gene for diabetic nephropathy?
Kaňková et al., Brno, Czech Republic. In Kidney Blood Press Res, 2012
BACKGROUND/AIMS: We have previously associated SNP 894G>T in the NOS3 gene with diabetic nephropathy (DN) using multi-locus analysis.
Genetic polymorphisms in oxidative stress pathway genes and modification of BMI and risk of non-Hodgkin lymphoma.
Zhang et al., New Haven, United States. In Cancer Epidemiol Biomarkers Prev, 2012
RESULTS: Polymorphisms in AKR1A1, AKR1C1, AKR1C3, CYBA, GPX1, MPO, NCF2, NCF4, NOS1, NOS2A NOS3, OGG1, ATG9B, SOD1, SOD2, SOD3, RAC1, and RAC2 genes after false discovery rate adjustment did not modify the association between BMI and risk of NHL overall and histologic subtypes.
Polymorphisms in autophagy genes and susceptibility to tuberculosis.
van Crevel et al., Nijmegen, Netherlands. In Plos One, 2011
No association was found between TB and polymorphisms in the genes ATG10, ATG16L2, ATG2B, ATG5, ATG9B, IRGM, LAMP1, LAMP3, P2RX7, WIPI1, MTOR and ATG4C.
Induction of cellular senescence by doxorubicin is associated with upregulated miR-375 and induction of autophagy in K562 cells.
Lin et al., Taiwan. In Plos One, 2011
Among the 24 human autophagy-related genes examined, a 12-fold increase of ATG9B at day 4 and a 20-fold increase of ATG18 at day 2 after DOX treatment were noted.
New insights into the function of Atg9.
Tooze et al., London, United Kingdom. In Febs Lett, 2010
The role of Atg9 trafficking in yeast and mammalian autophagy, is summarised.
Comprehensive analysis of expression pattern and promoter regulation of human autophagy-related genes.
Yoshida et al., Kawasaki, Japan. In Apoptosis, 2009
As a result, we observed a characteristic ubiquitous expression pattern for all the genes except for ATG2A, ATG9B, and WIPI2.
Effect of uncoupling endothelial nitric oxide synthase on calcium homeostasis in aged porcine endothelial cells.
Vilaine et al., Suresnes, France. In Cardiovasc Res, 2009
In aged cells with an uncoupled NOS3 as shown by the reduced BH(4) level, the increase in superoxide anion and the lower production of cGMP and the decrease in NO bioavailability were linearly correlated with the increase in basal [Ca(2+)](i).
Frameshift mutations of autophagy-related genes ATG2B, ATG5, ATG9B and ATG12 in gastric and colorectal cancers with microsatellite instability.
Lee et al., Seoul, South Korea. In J Pathol, 2009
In humans there are 16 known ATG genes, of which four (ATG2B, ATG5, ATG9B and ATG12) have mononucleotide repeats with seven or more nucleotides.
Disruption of nitric oxide synthase 3 protects against the cardiac injury, dysfunction, and mortality induced by doxorubicin.
Bloch et al., United States. In Circulation, 2007
CONCLUSIONS: These findings implicate NOS3 as a key mediator in the development of left ventricular dysfunction after administration of doxorubicin.
Hypoxia-inducible expression of a natural cis-antisense transcript inhibits endothelial nitric-oxide synthase.
Marsden et al., Toronto, Canada. In J Biol Chem, 2007
We demonstrate here that expression of sONE, also known as eNOS antisense (NOS3AS) or autophagy 9-like 2 (APG9L2), is robustly induced by hypoxia or functional deficiency of von Hippel-Lindau protein.
Endothelial nitric-oxide synthase antisense (NOS3AS) gene encodes an autophagy-related protein (APG9-like2) highly expressed in trophoblast.
Scherer et al., Toronto, Canada. In J Biol Chem, 2005
APG9L2 is highly expressed in placenta (trophoblast cells) and pituitary gland of adult tissues.
Salt intake, endothelial cell signaling, and progression of kidney disease.
Sanders, Birmingham, United States. In Hypertension, 2004
A balance is struck between TGF-beta1 and NOS3 as salt intake varies and creates a negative feedback loop, because TGF-beta1 increased expression of NOS3 and NO inhibited production of TGF-beta1 in healthy rats.
HLA-linked immune suppression in humans.
Nishimura et al., Fukuoka, Japan. In Immunol Suppl, 1988
There is no doubt that HLA-DR molecules are acting as the products of HLA-linked immune response genes (Ir-genes), because (i) HLA-DR molecules are the restriction elements in the interaction between CD4+ helper T cells and antigen-presenting cells (APC) to respond to many antigens such as streptococcal cell wall antigen (SCW) (Nishimura & Sasazuki, 1983; Sone et al., 1985; Hizayama et al., 1986), schistosomal antigen (Sj) (Hirayama et al., 1987), Mycobacterium leprae antigen (ML) (Kikuchi et al., 1986) and so on; and (ii) anti-HLA-DR monoclonal antibodies completely abolish the immune response to those antigens (Nishimura & Sasazuki, 1983; Sone et al., 1985).
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