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Aspartate beta-hydroxylase

junctin, AAH, ASPH
This gene is thought to play an important role in calcium homeostasis. The gene is expressed from two promoters and undergoes extensive alternative splicing. The encoded set of proteins share varying amounts of overlap near their N-termini but have substantial variations in their C-terminal domains resulting in distinct functional properties. The longest isoforms (a and f) include a C-terminal Aspartyl/Asparaginyl beta-hydroxylase domain that hydroxylates aspartic acid or asparagine residues in the epidermal growth factor (EGF)-like domains of some proteins, including protein C, coagulation factors VII, IX, and X, and the complement factors C1R and C1S. Other isoforms differ primarily in the C-terminal sequence and lack the hydroxylase domain, and some have been localized to the endoplasmic and sarcoplasmic reticulum. Some of these isoforms are found in complexes with calsequestrin, triadin, and the ryanodine receptor, and have been shown to regulate calcium release from the sarcoplasmic reticulum. Some isoforms have been implicated in metastasis. [provided by RefSeq, Sep 2009] (from NCBI)
Top mentioned proteins: Calsequestrin, Triadin, HAD, CAN, ACID
Papers on junctin
Deamidation reactions of protonated asparagine and glutamine investigated by ion spectroscopy.
Oomens et al., Nijmegen, Netherlands. In Rapid Commun Mass Spectrom, Mar 2016
We also confirm by IR spectroscopy that dehydration of protonated aspartic acid (AspH(+) ) and glutamic acid (GluH(+) ) leads to identical structures as to those found for the loss of NH3 from AsnH(+) and GlnH(+) .
Interleukin-1 and inflammasomes in ALD/AAH and NAFLD/NASH.
Szabo et al., Innsbruck, Austria. In Hepatology, Feb 2016
UNASSIGNED: Both alcoholic and non-alcoholic fatty liver diseases (ALD and NAFLD) are characterized by massive lipid accumulation in the liver accompanied by inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma in a substantial subgroup of patients.
Activation of signal transduction pathways during hepatic oncogenesis.
Wands et al., Providence, United States. In Cancer Lett, Feb 2016
Aspartate β-hydroxylase (ASPH) was found to link these upstream growth factor signaling pathways to downstream Notch activation in tumor tissues.
Aspartate β-hydroxylase modulates cellular senescence via glycogen synthase kinase 3β in hepatocellular carcinoma.
Wands et al., Providence, United States. In Hepatology, Jan 2016
BACKGROUND & AIMS: Aspartate β-hydroxylase (ASPH) is an enzyme overexpressed in human hepatocellular carcinoma (HCC) tumors and participates in the malignant transformation process.
Tobacco Smoke Exposure Impairs Brain Insulin/IGF Signaling: Potential Co-Factor Role in Neurodegeneration.
de la Monte et al., Providence, United States. In J Alzheimers Dis, Jan 2016
Correspondingly, CS and CS8+R exposures inhibited expression of proteins and phosphoproteins required for signaling through Akt, PRAS40, and/or p70S6K, increased AβPP-Aβ, and reduced ASPH protein, which is a target of insulin/IGF-1 signaling.
Junctate boosts phagocytosis by recruiting endoplasmic reticulum Ca2+ stores near phagosomes.
Nunes et al., Genève, Switzerland. In J Cell Sci, Dec 2015
Here, we tested whether junctate (also called ASPH isoform 8), a molecule that targets STIM1 to ER-plasma-membrane contacts upon Ca(2+)-store depletion, cooperates with STIM1 at phagosome junctions.
Immune dysfunction in acute alcoholic hepatitis.
Collins et al., Bristol, United Kingdom. In World J Gastroenterol, Dec 2015
Acute alcoholic hepatitis (AAH) is a serious complication of alcohol misuse and has high short term mortality.
Active Maintenance of the Gradient of Refractive Index Is Required to Sustain the Optical Properties of the Lens.
Donaldson et al., Auckland, New Zealand. In Invest Ophthalmol Vis Sci, Dec 2015
METHODS: One lens from a pair of bovine lenses was cultured in artificial aqueous humor (AAH), while the other was cultured in either AAH-High-K+ or AAH + 0.1 mM ouabain for 4 hours.
TNF-alpha modulates adipose macrophage polarization to M1 phenotype in response to scorpion venom.
Laraba-Djebari et al., Bab Ezzouar, Algeria. In Inflamm Res, Nov 2015
OBJECTIVE: We previously reported that Androctonus australis hector (Aah) venom and its toxic fraction affect adipose tissue metabolism.
Organization of junctional sarcoplasmic reticulum proteins in skeletal muscle fibers.
Rossi et al., Siena, Italy. In J Muscle Res Cell Motil, Oct 2015
At the j-SR, several trans-membrane proteins like triadin, junctin, or intra-luminal SR proteins like calsequestrin, are assembled together with the ryanodine receptor, the SR Ca(2+) release channel, into a macromolecular complex specialized in releasing Ca(2+).
Involvement of Kallikrein-Kinin System on Cardiopulmonary Alterations and Inflammatory Response Induced by Purified Aah I Toxin from Scorpion Venom.
Laraba-Djebari et al., Bab Ezzouar, Algeria. In Inflammation, Oct 2015
This study was performed to evaluate cardiopulmonary damages and inflammatory response on injected rats with Aah I toxin of scorpion venom and the involvement of Kallikrein-Kinin system in this pathogenesis.
Potential Role of Phosphorylation as a Regulator of Aspartyl-(asparaginyl)-β-hydroxylase: Relevance to Infiltrative Spread of Human Hepatocellular Carcinoma.
de la Monte et al., Providence, United States. In Liver Cancer, Sep 2015
Abundant expression of aspartyl-(asparaginyl)-β-hydroxylase (AAH) correlates with infiltrative growth of hepatocellular carcinoma (HCC).
The disorders of the calcium release unit of skeletal muscles: what have we learned from mouse models?
Cancellara et al., Padova, Italy. In J Muscle Res Cell Motil, Feb 2015
The release from the Sarcoplasmic Reticulum stores (SR) is handled by a multiprotein complex called Calcium Release Unit and composed of DiHydroPyridine Receptor or DHPR, Ryanodine Receptor or RYR, Calsequestrin or CASQ, junctin, Triadin, Junctophilin and Mitsugumin 29.
The aspartyl (asparaginyl) beta-hydroxylase in carcinomas.
Shi et al., In Front Biosci, 2014
Aspartyl-(asparaginyl)-β-hydroxylase (AAH) is a member of the α-ketoglutarate-dependent dioxygenase family that catalyzes the hydroxylation of aspartyl and asparaginyl residues epidermal growth factor (EGF)-like domains of protein.
Early lung cancer with lepidic pattern: adenocarcinoma in situ, minimally invasive adenocarcinoma, and lepidic predominant adenocarcinoma.
Warth et al., Heidelberg, Germany. In Curr Opin Pulm Med, 2014
PURPOSE OF REVIEW: This review gives a comprehensive overview on recent developments in the classification of neoplastic lung lesions with lepidic growth patterns, comprising the adenocarcinoma (ADC) precursor lesions atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ (AIS), and minimally invasive adenocarcinoma (MIA) as well as lepidic predominant adenocarcinoma (LPA).
Junctate is a Ca2+-sensing structural component of Orai1 and stromal interaction molecule 1 (STIM1).
Gwack et al., Los Angeles, United States. In Proc Natl Acad Sci U S A, 2012
Data show that junctate (ASPH) is an interacting partner of Orai1-STIM1 complex.
Role of Junctin protein interactions in cellular dynamics of calsequestrin polymer upon calcium perturbation.
Kwon et al., Taejŏn, South Korea. In J Biol Chem, 2012
Ca(2+) and JNT-dependent disassembly of the CSQ2 polymer
Dual role of junctin in the regulation of ryanodine receptors and calcium release in cardiac ventricular myocytes.
Valdivia et al., Madison, United States. In J Physiol, 2012
Results predict that junctin ablation, or mutations that alter its structural attributes, may mimic the etiology of catecholaminergic polymorphic ventricular tachycardia by causing enhanced diastolic Ca2+ leak in the presence of beta-adrenergic activation.
Triadin/Junctin double null mouse reveals a differential role for Triadin and Junctin in anchoring CASQ to the jSR and regulating Ca(2+) homeostasis.
Perez et al., Chieti, Italy. In Plos One, 2011
in skeletal muscle the disruption of Tdn/CASQ link has a more profound effect on jSR architecture and myoplasmic Ca(2+) regulation than Jct/CASQ association.
siRNA inhibition of aspartyl-asparaginyl β-hydroxylase expression impairs cell motility, Notch signaling, and fetal growth.
de la Monte et al., Providence, United States. In Pathol Res Pract, 2011
Aspartyl-asparaginyl-beta-hydroxylase is an important, positive regulator of trophoblastic cell motility, and it's inhibition in vivo leads to impaired implantation and fetal growth, and alters Notch-signaling mechanisms.
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