Human Histidyl-TRNA Synthetase [His] (DAG603)

Human Histidyl-TRNA Synthetase [His], recombinant protein from Baculovirus

Product Overview
Recombinanthuman histidyl-tRNA synthetase (Jo-1) full-length cDNA coding fused to ahexa-histidine purification tag. Expressed by recombinant baculovirus(Autographa californica multiple nuclear polyhedrosis virus; AcMNPV)infection of Spodoptera frugiperda
Nature
Recombinant
Tag/Conjugate
His
Procedure
None
Purity
> 90%(SDS-PAGE).
Concentration
0.7-1.0 μg/ml(depending on the type of ELISA plate and coating buffer). Suitable forbiotinylation and iodination.
Buffer
Ionicstrength between 200 and 250 mM salt, neutral to slightly alkaline pH and 20%glycerol as cryoprotective agent.
Preservative
None
Storage
2-8°C short term, -20°C long term
Introduction
Aminoacyl-tRNA synthetases are a class of enzymes that charge tRNAs with their cognate amino acids. The protein encoded by this gene is a cytoplasmic enzyme which belongs to the class II family of aminoacyl-tRNA synthetases. The enzyme is responsible for the synthesis of histidyl-transfer RNA, which is essential for the incorporation of histidine into proteins. The gene is located in a head-to-head orientation with HARSL on chromosome five, where the homologous genes share a bidirectional promoter. The gene product is a frequent target of autoantibodies in the human autoimmune disease polymyositis/dermatomyositis. Several transcript variants encoding different isoforms have been found for this gene.
Antigen Description
Aminoacyl-tRNAsynthetases are a class of enzymes that charge tRNAs with their cognate aminoacids. The protein encoded by this gene is a cytoplasmic enzyme which belongsto the class II family of aminoacyl-tRNA synthetases. The enzyme isresponsible for the synthesis of histidyl-transfer RNA, which is essentialfor the incorporation of histidine into proteins. The gene is located in ahead-to-head orientation with HARSL on chromosome five, where the homologousgenes share a bidirectional promoter. The gene product is a frequent targetof autoantibodies in the human autoimmune diseasepolymyositis/dermatomyositis.
Keywords
HARS; histidyl-tRNA synthetase; histidyl-tRNA synthetase, cytoplasmic; histidine tRNA ligase 1; cytoplasmic; EC 6.1.1.21; FLJ20491; HisRS; histidine translase; Histidine tRNA ligase; Histidyl tRNA synthetase; HRS; Human histidyl tRNA synthetase homolog (H

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References


Efficacy of tibolone and transdermal estrogen therapy on psychological symptoms in women following surgical menopause

INTERNATIONAL JOURNAL OF GYNECOLOGY & OBSTETRICS

Authors: Baksu, A; Ayas, B; Citak, S; Kalan, A; Baksu, B; Goker, N

Objective: This study investigated the efficacy of tibolone and transdermal estradiol therapy on menopausal and psychological symptoms in women following surgical menopause. Method: Seventy-five women who had undergone surgical menopause were randomized to a 6-month double-blind interventional study treatment with oral 2.5 mg/day tibolone, transdermal 3.9 mg/week estradiol or oral placebo. The patients were assessed using Kupperman's Scale, Hamilton Depression Rating Scale (HDRS) and Hamilton Anxiety Rating Scale (HARS) before and at the end of the 6 months of treatment. Result: Sixty-five subjects completed the study: 23 on tibolone, 21 on transdermal estradiol and 21 on placebo. At the end of the 6 months of therapy, highly significant improvements in menopausal symptoms, depression and anxiety scores were observed in both groups (tibolone and transdermal estradiol groups) as compared with baseline values (p < 0.001). However, in the placebo group, there were no significant differences on changes from baseline to the end of treatment (p > 0.05). Conclusion: These results suggest that tibolone and transdermal estradiol therapy significantly improve menopausal and psychological symptoms in women following surgical menopause. (c) 2005 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved.

Preliminary evidence of riluzole efficacy in antidepressant-treated patients with residual depressive symptoms

BIOLOGICAL PSYCHIATRY

Authors: Sanacora, Gerard; Kendell, Steven F.; Levin, Yael; Simen, Arthur A.; Fenton, Lisa R.; Coric, Vladimir; Krystal, John H.

Background: Excessive glutamatergic neurotransmission may contribute to the pathophysiology of major depressive disorder (MDD). Recent evidence suggests that riluzole and other agents that target glutamate neurotransmission may show antidepressant activity. Methods: Ten patients with treatment-resistant depression had riluzole added to their ongoing medication regimen for 6 weeks, followed by an optional 6-week continuation phase. Depression and anxiety severity were assessed using the Hamilton Depression Rating Scale (HDRS) and the Hamilton Anxiety Rating Scale (HARS). Linear mixed models were used to test for a linear trend in HDRS and HARS scores across time with treatment. Results: Subjects' HDRS and HARS scores declined significantly following the initiation of riluzole augmentation therapy. The effect of riluzole was significant at the end of the first week of treatment and persisted for the 12-week duration of the study. Conclusions: These data suggest that riluzole augmentation produces antidepressant and anxiolytic effects inpatients with treatment-resistant depression.

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