Institution
Central Drug Research Institute
Facility•Lucknow, Uttar Pradesh, India•
About: Central Drug Research Institute is a facility organization based out in Lucknow, Uttar Pradesh, India. It is known for research contribution in the topics: Leishmania donovani & Brugia malayi. The organization has 4357 authors who have published 7257 publications receiving 143871 citations. The organization is also known as: Central Drug Research Institute, Lucknow & CDRI.
Papers published on a yearly basis
Papers
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TL;DR: The synthesis of a series of benzocoumarin keto-enamine schiff bases is reported, which significantly lowered the plasma triglyceride levels, total cholesterol and total cholesterol levels, and accompanied by an increase in HDL-C/TC ratio in hyperlipidemic hamsters to a greater degree than the reference drugs atorvastatin and lovastatin.
51 citations
TL;DR: It is shown that whilst SPINK1 is transcriptionally repressed by androgen receptor and its co-repressor REST, it is upregulated after androgen-deprivation therapy, which leads to neuroendocrine differentiation of prostate cancer cells.
Abstract: Emergence of an aggressive androgen receptor (AR)-independent neuroendocrine prostate cancer (NEPC) after androgen-deprivation therapy (ADT) is well-known. Nevertheless, the majority of advanced-stage prostate cancer patients, including those with SPINK1-positive subtype, are treated with AR-antagonists. Here, we show AR and its corepressor, REST, function as transcriptional-repressors of SPINK1, and AR-antagonists alleviate this repression leading to SPINK1 upregulation. Increased SOX2 expression during NE-transdifferentiation transactivates SPINK1, a critical-player for maintenance of NE-phenotype. SPINK1 elicits epithelial-mesenchymal-transition, stemness and cellular-plasticity. Conversely, pharmacological Casein Kinase-1 inhibition stabilizes REST, which in cooperation with AR causes SPINK1 transcriptional-repression and impedes SPINK1-mediated oncogenesis. Elevated levels of SPINK1 and NEPC markers are observed in the tumors of AR-antagonists treated mice, and in a subset of NEPC patients, implicating a plausible role of SPINK1 in treatment-related NEPC. Collectively, our findings provide an explanation for the paradoxical clinical-outcomes after ADT, possibly due to SPINK1 upregulation, and offers a strategy for adjuvant therapies.
51 citations
TL;DR: It is suggested that CC-treatment at higher doses specifically induces cellular apoptosis and inhibits cellular proliferation; whereas at lower doses, it inhibits cellular migration and invasion.
51 citations
TL;DR: In this paper, the reaction of aldehydes with 2−aminophenol and O−phenylenediamines in the presence of iodine was used to synthesize 2−Arylbenzoxazoles and 2−arylbenzimidazoles.
51 citations
TL;DR: It may be suggested that impairment of neuromuscular coordination is inked to oxidative stress rather than mitochondrial enzyme deficiency, all the processes are correlated with each other with the progression of time.
51 citations
Authors
Showing all 4385 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| Sanjay Kumar | 120 | 2052 | 82620 |
| John A. Katzenellenbogen | 95 | 691 | 36132 |
| Brajesh K. Singh | 83 | 401 | 24101 |
| Gaurav Sharma | 82 | 1244 | 31482 |
| Sudhir Kumar | 82 | 524 | 216349 |
| Pramod K. Srivastava | 79 | 390 | 27330 |
| Mohan K. Raizada | 75 | 473 | 21452 |
| Syed F. Ali | 71 | 446 | 18669 |
| Ravi Shankar | 66 | 672 | 19326 |
| Ramesh Chandra | 66 | 620 | 16293 |
| Manoj Kumar | 65 | 408 | 16838 |
| Manish Kumar | 61 | 1425 | 21762 |
| Anil Kumar Saxena | 58 | 310 | 10107 |
| Sanjay Krishna | 56 | 624 | 13731 |
| Naibedya Chattopadhyay | 56 | 242 | 9795 |