Search

Your search keyword '"Basu, Reetobrata"' showing total 64 results
Start Over Author "Basu, Reetobrata"
64 results on '"Basu, Reetobrata"'

52. SAT-LB054 Growth Hormone Receptor (GHR) Antagonism Suppresses Hepatocellular Carcinoma Growth in a Syngeneic Mouse Model

Author

Mathes, Samuel, primary, Qian, Yanrong, additional, Basu, Reetobrata, additional, Arnett, Nathan, additional, Duran Ortiz, Silvana, additional, Kruse, Colin, additional, Brittain, Alison, additional, Funk, Kevin, additional, Terry, Joseph, additional, Smith, Cole, additional, Bell, Stephen, additional, List, Edward, additional, Berryman, Darlene, additional, and Kopchick, John, additional

Published
2019
Full Text
View/download PDF

53. SAT-041 Bioinformatic Analysis of Human Cutaneous Melanomas Identifies Increased Mortality and Genetic Alterations in GH-responsive Tumors

Author

Kruse, Colin P.S., primary, Basu, Reetobrata, additional, Qian, Yanrong, additional, Young, Jonathan, additional, Kruse, Hans, additional, Brittain, Alison, additional, Duran Ortiz, Silvana, additional, Jensen, Elizabeth, additional, Bell, Stephen, additional, Buchman, Mathew, additional, and Kopchick, John, additional

Published
2019
Full Text
View/download PDF

54. MON-311 GH Action Upregulates ABC Transporters And EMT Markers In A Syngeneic Melanoma Mouse Model

Author

Qian, Yanrong, primary, Basu, Reetobrata, additional, Mathes, Samuel, additional, Arnett, Nathan, additional, Duran-Ortiz, Silvana, additional, Kruse, Colin, additional, Brittain, Alison, additional, Funk, Kevin, additional, Terry, Joseph, additional, Smith, Cole, additional, Henry, Brooke, additional, Bell, Stephen, additional, List, Edward, additional, Berryman, Darlene, additional, and Kopchick, John, additional

Published
2019
Full Text
View/download PDF

58. Lessons from growth hormone receptor gene-disrupted mice: are there benefits of endocrine defects?

Author

Basu, Reetobrata, Yanrong Qian, and Kopchick, John J.

Subjects
*ENDOCRINE diseases, *SOMATOTROPIN receptors, *HORMONE therapy, *HORMONE resistance, *LABORATORY mice, *LARON dwarfism
Abstract

Growth hormone (GH) is produced primarily by anterior pituitary somatotroph cells. Numerous acute human (h) GH treatment and long-term follow-up studies and extensive use of animal models of GH action have shaped the body of GH research over the past 70 years. Work on the GH receptor (R)-knockout (GHRKO) mice and results of studies on GH-resistant Laron Syndrome (LS) patients have helped define many physiological actions of GH including those dealing with metabolism, obesity, cancer, diabetes, cognition and aging/longevity. In this review, we have discussed several issues dealing with these biological effects of GH and attempt to answer the question of whether decreased GH action may be beneficial. [ABSTRACT FROM AUTHOR]

Published
2018
Full Text
View/download PDF

59. Optimization of Pyrrolamides as Mycobacterial GyrB ATPase Inhibitors: Structure-Activity Relationship andIn VivoEfficacy in a Mouse Model of Tuberculosis

Author

P, Shahul Hameed, primary, Solapure, Suresh, additional, Mukherjee, Kakoli, additional, Nandi, Vrinda, additional, Waterson, David, additional, Shandil, Radha, additional, Balganesh, Meenakshi, additional, Sambandamurthy, Vasan K., additional, Raichurkar, Anand Kumar, additional, Deshpande, Abhijeet, additional, Ghosh, Anirban, additional, Awasthy, Disha, additional, Shanbhag, Gajanan, additional, Sheikh, Gulebahar, additional, McMiken, Helen, additional, Puttur, Jayashree, additional, Reddy, Jitendar, additional, Werngren, Jim, additional, Read, Jon, additional, Kumar, Mahesh, additional, R, Manjunatha, additional, Chinnapattu, Murugan, additional, Madhavapeddi, Prashanti, additional, Manjrekar, Praveena, additional, Basu, Reetobrata, additional, Gaonkar, Sheshagiri, additional, Sharma, Sreevalli, additional, Hoffner, Sven, additional, Humnabadkar, Vaishali, additional, Subbulakshmi, Venkita, additional, and Panduga, Vijender, additional

Published
2014
Full Text
View/download PDF

60. Optimization of Pyrrolamides as Mycobacterial GyrB ATPase Inhibitors: Structure-Activity Relationship and In Vivo Efficacy in a Mouse Model of Tuberculosis

Author

P, Shahul Hameed, primary, Solapure, Suresh, additional, Mukherjee, Kakoli, additional, Nandi, Vrinda, additional, Waterson, David, additional, Shandil, Radha, additional, Balganesh, Meenakshi, additional, Sambandamurthy, Vasan K., additional, Raichurkar, Anand Kumar, additional, Deshpande, Abhijeet, additional, Ghosh, Anirban, additional, Awasthy, Disha, additional, Shanbhag, Gajanan, additional, Sheikh, Gulebahar, additional, McMiken, Helen, additional, Puttur, Jayashree, additional, Reddy, Jitendar, additional, Werngren, Jim, additional, Read, Jon, additional, Kumar, Mahesh, additional, R, Manjunatha, additional, Chinnapattu, Murugan, additional, Madhavapeddi, Prashanti, additional, Manjrekar, Praveena, additional, Basu, Reetobrata, additional, Gaonkar, Sheshagiri, additional, Sharma, Sreevalli, additional, Hoffner, Sven, additional, Humnabadkar, Vaishali, additional, Subbulakshmi, Venkita, additional, and Panduga, Vijender, additional

Published
2014
Full Text
View/download PDF

61. Optimization of Pyrrolamides as Mycobacterial GyrB ATPase Inhibitors: Structure-Activity Relationship and In VivoEfficacy in a Mouse Model of Tuberculosis

Author

P, Shahul Hameed, Solapure, Suresh, Mukherjee, Kakoli, Nandi, Vrinda, Waterson, David, Shandil, Radha, Balganesh, Meenakshi, Sambandamurthy, Vasan K., Raichurkar, Anand Kumar, Deshpande, Abhijeet, Ghosh, Anirban, Awasthy, Disha, Shanbhag, Gajanan, Sheikh, Gulebahar, McMiken, Helen, Puttur, Jayashree, Reddy, Jitendar, Werngren, Jim, Read, Jon, Kumar, Mahesh, R, Manjunatha, Chinnapattu, Murugan, Madhavapeddi, Prashanti, Manjrekar, Praveena, Basu, Reetobrata, Gaonkar, Sheshagiri, Sharma, Sreevalli, Hoffner, Sven, Humnabadkar, Vaishali, Subbulakshmi, Venkita, and Panduga, Vijender

Abstract

ABSTRACTMoxifloxacin has shown excellent activity against drug-sensitive as well as drug-resistant tuberculosis (TB), thus confirming DNA gyrase as a clinically validated target for discovering novel anti-TB agents. We have identified novel inhibitors in the pyrrolamide class which kill Mycobacterium tuberculosisthrough inhibition of ATPase activity catalyzed by the GyrB domain of DNA gyrase. A homology model of the M. tuberculosisH37Rv GyrB domain was used for deciphering the structure-activity relationship and binding interactions of inhibitors with mycobacterial GyrB enzyme. Proposed binding interactions were later confirmed through cocrystal structure studies with the Mycobacterium smegmatisGyrB ATPase domain. The most potent compound in this series inhibited supercoiling activity of DNA gyrase with a 50% inhibitory concentration (IC50) of <5 nM, an MIC of 0.03 μg/ml against M. tuberculosisH37Rv, and an MIC90of <0.25 μg/ml against 99 drug-resistant clinical isolates of M. tuberculosis. The frequency of isolating spontaneous resistant mutants was ∼10−6to 10−8, and the point mutation mapped to the M. tuberculosisGyrB domain (Ser208 Ala), thus confirming its mode of action. The best compound tested for in vivoefficacy in the mouse model showed a 1.1-log reduction in lung CFU in the acute model and a 0.7-log reduction in the chronic model. This class of GyrB inhibitors could be developed as novel anti-TB agents.

Published
2013
Full Text
View/download PDF

62. Growth Hormone Receptor in Melanoma: A Unique Approach to Therapy

Author

Basu, Reetobrata

Subjects
Molecular Biology, Endocrinology, Oncology, Biology, Biochemistry, melanoma, growth hormone, growth hormone receptor, drug resistance, GH, GHR, cancer, melanogenesis, MITF, EMT, ABC transporters, RNAi, chemotherapy
Abstract

Human melanomas are one of the most therapy resistant types of cancer, expressing a repertoire of mechanisms for drug resistance. Intracellular signaling networks used by the melanoma cells for active proliferation, migration, invasion, therapy resistance and metastases happen to strongly overlap with those regulated by the human growth hormone (hGH). Indeed consistently high levels of GH receptor (GHR) expression have been observed in almost all melanoma cell lines in the NCI60 human cancer panel. There are no comprehensive studies investigating the effects of GH action or GHR antagonism on the GH-responsive intracellular signaling pathways and downstream effects in human melanoma. Here we report for the first time, a detailed analysis of the effect of siRNA mediated GHR knock-down (KD) and effect of hGH on the intracellular signaling and downstream phenotypes in human melanoma cells. We report the existence of an autocrine loop of hGH-GHR in the aforesaid human melanoma cell lines, changes observed in relevant intracellular signaling pathways, RNA transcript level changes observed in multiple key modulators of the GH/GHR axis. Phosphorylation states of the JAK2, SRC, STAT1, 3, and 5, p44/42-MAPK, AKT and mTOR increased in a dose-dependent manner with hGH stimulation and were significantly attenuated by GHR-KD. Differential yet significant changes were observed in the relative mRNA transcript levels of prolactin (PRL), insulin and related growth factors (IGF1, IGF2) and their receptors, following hGH treatment or GHR-KD. Thus, the GH/GHR interaction can influence the levels of the JAK2, SRC, STAT1, 3, and 5, p44/42-MAPK, AKT and mTOR in human melanoma cells and may provide leads as to potential targets for therapeutic intervention.

Published
2016

63. Optimization of Pyrrolamides as Mycobacterial GyrB ATPase Inhibitors: Structure-Activity Relationship and In VivoEfficacy in a Mouse Model of Tuberculosis

Author

P, Shahul Hameed, Solapure, Suresh, Mukherjee, Kakoli, Nandi, Vrinda, Waterson, David, Shandil, Radha, Balganesh, Meenakshi, Sambandamurthy, Vasan K., Raichurkar, Anand Kumar, Deshpande, Abhijeet, Ghosh, Anirban, Awasthy, Disha, Shanbhag, Gajanan, Sheikh, Gulebahar, McMiken, Helen, Puttur, Jayashree, Reddy, Jitendar, Werngren, Jim, Read, Jon, Kumar, Mahesh, R, Manjunatha, Chinnapattu, Murugan, Madhavapeddi, Prashanti, Manjrekar, Praveena, Basu, Reetobrata, Gaonkar, Sheshagiri, Sharma, Sreevalli, Hoffner, Sven, Humnabadkar, Vaishali, Subbulakshmi, Venkita, and Panduga, Vijender

Published
2014
Full Text
View/download PDF

64. Investigating Amine Oxidase Domain Containing Genes - amx-1 and amx-2 - in Caenorhabditis elegans

Author

Basu, Reetobrata

Subjects
Animal Sciences, Behavioral Sciences, Biochemistry, Experiments, Genetics, Molecular Biology, Neurobiology, Neurology, Neurosciences, amx, Caenorhabditis elegans, monoamine oxidase, histone demethylase, monoamine, Reetobrata Basu, Janet Duerr, AMX, MAO, HDM, worm
Abstract

Monoamine (MA) neurotransmitters affect multiple behaviors in animals. MA homeostasis is achieved partly by monoamine-oxidase (MAO) enzymes - a drug target for many human neuropsychiatric disorders. In C. elegans the MA pathway is similar to that in humans and the worm shows MA dependent behaviors, affected by MAO inhibitor (MAOI) treatments. We cloned, expressed and purified the C. elegans genes - amx-1 and amx-2 in heterologous systems. Absorption spectra indicated that AMX1 and AMX2 bind the redox cofactor flavin adenine dinucleotide (FAD). Biochemical assays with wild-type (N2) or mutant worm lysates showed significant differences in MAO and histone demethylase (HDM) activities between them. Purified AMX1 and AMX2 had very low in vitro HDM activity independently, but both significantly increased the HDM activity of worm lysates. AMX1 had negligible in vitro MAO activity, whereas AMX2 had high in vitro MAO activity, with substrate and inhibitor specificities.

Published
2014

Catalog

Books, media, physical & digital resources
See catalog results