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<title>CSIR-CDRI Publications</title>
<link>http://dkr.cdri.res.in:8080/xmlui/handle/123456789/7</link>
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<rdf:li rdf:resource="http://dkr.cdri.res.in:8080/xmlui/handle/1/1719"/>
<rdf:li rdf:resource="http://dkr.cdri.res.in:8080/xmlui/handle/1/1718"/>
<rdf:li rdf:resource="http://dkr.cdri.res.in:8080/xmlui/handle/1/1712"/>
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<dc:date>2026-04-19T12:10:48Z</dc:date>
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<title>Krc</title>
<link>http://dkr.cdri.res.in:8080/xmlui/handle/1/1719</link>
<description>Krc
sheikh, Arshi
Tuberculosis, 1,2,3-Triazoles, antimycobacterial activity, molecular docking
Tuberculosis, 1,2,3-Triazoles, antimycobacterial activity, molecular docking
</description>
<dc:date>2016-01-01T00:00:00Z</dc:date>
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<item rdf:about="http://dkr.cdri.res.in:8080/xmlui/handle/1/1718">
<title>Synthesis and Biological Evaluation of Novel 1,2,3-Triazole derivatives as Anti-TB Agents</title>
<link>http://dkr.cdri.res.in:8080/xmlui/handle/1/1718</link>
<description>Synthesis and Biological Evaluation of Novel 1,2,3-Triazole derivatives as Anti-TB Agents
Ali, Abdul A.; Gogoi, Dhrubajyoti; Buragohain, Alak K.; Saikia, Prakash J.; Gehlot, Praveen S; Kumar, Arvind; Trivedi, Priyanka; Chaturvedi, Vinita; Sarma, Diganta
A series of seventeen novel 1,2,3-Triazole derivatives were efficiently synthesized in excellent yields by the popular ‘click chemistry’ approach and evaluated for their in vitro anti-tubercular activity against Mycobacterium tuberculosis H37Ra. Molecular docking of the target compounds into the active site of DprE1 (Decaprenylphosphoryl-β-D-ribose-2′-epimerase) enzyme revealed significant structural information on the plausible binding interactions
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<dc:date>2016-01-01T00:00:00Z</dc:date>
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<item rdf:about="http://dkr.cdri.res.in:8080/xmlui/handle/1/1712">
<title>4‐Hydroxyisoleucine ameliorates fatty acid‐induced insulin resistance and inflammatory response in skeletal muscle cells</title>
<link>http://dkr.cdri.res.in:8080/xmlui/handle/1/1712</link>
<description>4‐Hydroxyisoleucine ameliorates fatty acid‐induced insulin resistance and inflammatory response in skeletal muscle cells
Maurya, C K; Singh, Rohit; Jaiswal, Natasha; Venkateswarlu, K; Narender, Tadigoppula; Tamrakar, A K
The 4‐Hydroxyisoleucine (4‐HIL), an unusual amino acid isolated from the seeds of Trigonella foenum‐graecum was investigated for the metabolic effects to ameliorate free fatty acid‐induced insulin resistance in skeletal muscle cells. An incubation of L6 myotubes with palmitate inhibited insulin stimulated‐ glucose uptake and ‐translocation of glucose transporter 4 (GLUT4) to cell surface. Addition of 4‐HIL strongly prevented this inhibition. We then examined insulin signaling pathway, where 4‐HIL effectively inhibited the ability of palmitate to reduce insulin‐stimulated phosphorylation of insulin receptor substrate‐1(IRS‐1), protein kinase B (PKB/AKT), AKT substrate of 160 KD (AS160) and glycogen synthase kinase 3β (GSK‐3 β) in L6 myotubes. Moreover, 4‐HIL presented strong inhibition on palmitate‐induced production of reactive oxygen species (ROS) and associated inflammation, as the activation of NF‐κB and, JNK1/2, ERK1/2 and p38 MAPK was greatly reduced. 4‐HIL also inhibited inflammation‐stimulated IRS‐1 serine phosphorylation and restored insulin‐stimulated IRS‐1 tyrosine phosphorylation in presence of palmitate, leading to enhanced insulin sensitivity. These findings suggested that 4‐HIL could inhibit palmitate‐induced, ROS‐associated inflammation and restored insulin sensitivity through regulating IRS‐1 function. 
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<dc:date>2014-01-01T00:00:00Z</dc:date>
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<item rdf:about="http://dkr.cdri.res.in:8080/xmlui/handle/1/1705">
<title>Cofactor Biosynthetic Pathways in Mycobacterium tuberculosisas Potential Drug Targets</title>
<link>http://dkr.cdri.res.in:8080/xmlui/handle/1/1705</link>
<description>Cofactor Biosynthetic Pathways in Mycobacterium tuberculosisas Potential Drug Targets
Pandey, Shilpika; Gaur, Sarthak; Topno, Neha; Chopra, Sidharth; Dasgupta, Arunava
There are many chemotherapeutic interventions available for tuberculosis (TB) and are in use for more than five decades, but still there is an urgent need for novel drugs against new targets due to emergence of resistant strains. Moreover, the ability of Mycobacterium tuberculosis(Mtb) to survive within granulomas in a non-replicating latent stage prolongs the course of drug dose and hence increases the severity of the disease. The significant rerouting of metabolism is one of the key processes that help mycobacteria adapt to the hostile environment of host granuloma. In this review, we are focusing on some of the cofactor biosynthetic pathways of Mycobacterium tuberculosisand their utilization as drug targets.
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<dc:date>2014-01-01T00:00:00Z</dc:date>
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