Articles written in Journal of Biosciences
Volume 20 Issue 5 December 1995 pp 665-673
The estrogen agonistic and antagonistic properties of clomiphene citrate were investigated in the mice. Clomiphene citrate was tested at various doses of 0.1, 1.0, 10 and 100 μg for three consecutive days in immature and mature bilaterally ovariectomized mice. Clomiphene citrate showed uterotrophic activity in both immature and ovariectomized conditions. The lower doses of 0.1 and 1.0 μg were ineffective to show any uterotrophic stimulation. Clomiphene citrate at 10 μg dose produced 305.56% increase in uterine weight i.e., 27.70 ± 0.24 vs 6.83 ± 0.06 in immature and 182.27% i.e., 42.68 ± 1.12 vs 15.12 ± 0.57 in ovariectomized mice. Clomiphene citrate at 100 μg dose showed significant uterotrophic effect e.g., 435.57% i.e., 36.58 ±0.34 vs 6.83 ± 0.06 in immature and 586% i.e., 103.80 ± 0.60 in ovariectomized mice. When clomiphene citrate was administered in combination with 0.32 μg of estradiol 17-β it caused significant antagonistic effect (decrease in uterine weight) at 10 and 100 μg respectively. Clomiphene citrate at 10 μg dose produced 32% i.e., 28.93 ± 0.43 vs 38.04 ± 2.68 in immature and 35% i.e., 59.64±1.44 vs 83.34 ±0.25 in ovariectomized mice respectively. Histological observation clearly showed that clomiphene citrate at 10 and 100 μg doses did not cause any differential hypertrophy of the epithelial layer. Similar doses in combination with estradiol produced significant antagonistic effect on uterine weight and luminal epithelial cell height.
Volume 24 Issue 1 March 1999 pp 4-6 Clipboard
Volume 24 Issue 2 June 1999 pp 233-240 Articles
Air borne insects, mostly carried by wind currents, were trapped over the northern Arabian sea (16‡ to 20‡ N; 68‡ to 72‡ E), in the course of cruise No. 111, ORV
Volume 25 Issue 3 September 2000 pp 213-214 Clipboard
Volume 25 Issue 4 December 2000 pp 315-316 Clipboard
Volume 26 Issue 1 March 2001 pp 3-5 Clipboard
Volume 26 Issue 3 September 2001 pp 285-287 Clipboard
Volume 27 Issue 7 December 2002 pp 629-632 Clipboard
Volume 42 Issue 1 March 2017 pp 57-68 Article
DNA methylation, mediated by double-stranded RNA, is a conserved epigenetic phenomenon that protects a genome fromtransposons, silences unwanted genes and has a paramount function in plant or animal development. Methyl CpG bindingdomain proteins are members of a class of proteins that bind tomethylated DNA. The Arabidopsis thaliana genome encodes13 methyl CpG binding domain (MBD) proteins, but themolecular/biological functions of most of these proteins are still notclear. In the present study, we identified four proteins that interact with AtMBD6. Interestingly, three of them contain RNAbinding domains and are co-localized with AtMBD6 in the nucleus. The interacting partners includes AtRPS2C (a 40Sribosomal protein), AtNTF2 (nuclear transport factor 2) and AtAGO4 (Argonoute 4). The fourth protein that physicallyinteracts with AtMBD6 is a histone-modifying enzyme, histone deacetylase 6 (AtHDA6), which is a known component ofthe RNA-mediated gene silencing system. Analysis of genomic DNA methylation in the atmbd6, atrps2c and atntf2mutants, using methylation-sensitive PCR detected decreased DNA methylation at miRNA/siRNA producing loci,pseudogenes and other targets of RNA-directed DNA methylation. Our results indicate that AtMBD6 is involved inRNA-mediated gene silencing and it binds to RNA binding proteins like AtRPS2C, AtAGO4 and AtNTF2. AtMBD6 alsointeracts with histone deacetylase AtHDA6 that might have a role in chromatin condensation at the targets of RdDM.
Volume 44 Issue 1 March 2019 Article ID 0014 Article
DNA methylation is an important epigenetic modification that governs transcriptional regulation. The methylation mark isread by a special class of proteins called methyl-CpG-binding domain proteins. The role of DNA methylation has beenfound in X-chromosome inactivation, genomic imprinting, transposon silencing, and self-incompatibility. Recently,remodeling of global DNA methylation was demonstrated in Arabidopsis during low phosphate availability. The presentstudy reports that AtMBD4 gene of Arabidopsis negatively regulates phosphate starvation. The T-DNA insertion mutation atthe AtMBD4 locus exhibited altered root architecture as compared to wild-type plants. Using microarray hybridization andanalysis, an increased transcript accumulation of 242 genes was observed in the mutant. Many of these genes were relatedto phosphate transporters and transcription factors, involved in phosphate starvation response. Comparison of data ofatmbd4 mutant with publicly available microarray data of phosphate starvation response indicated the role of AtMBD4protein in phosphate starvation response. Further, promoter analysis of up-regulated genes suggested that cis-regulatoryelements like MBS, W-box, and B1BS are more prominent in the promoters of up-regulated genes. Upon performing amethylation-specific PCR, a decreased DNA methylation in the promoter regions of up-regulated genes was observed. Theaccumulation of anthocyanin and inorganic phosphate in the atmbd4 mutant was found to be higher than the wild-typeplant. Altered root morphology, up-regulation of phosphate starvation-induced genes in atmbd4 mutant suggests thatAtMBD4 negatively regulates the phosphate starvation response.
Volume 44 Issue 6 December 2019 Article ID 0147 Article
The Aurora kinases represent a group of serine/threonine kinases which are crucial regulators of mitosis. DysregulatedAurora kinase B (AurkB) expression, stemming from genomic amplification, increased gene transcription or overexpressionof its allosteric activators, is capable of initiating and sustaining malignant phenotypes. Although AurkB level in cells iswell-orchestrated, studies that relate to its stability or activity, independent of mitosis, are lacking. We report that AurkBundergoes acetylation in vitro by lysine acetyltransferases (KATs) belonging to different families, namely by p300 andTip60. The haploinsufficient tumor suppressor Tip60 acetylates two highly conserved lysine residues within the kinasedomain of AurkB which not only impinges the protein stability but also its kinase activity. These results signify a probableoutcome on the increase in ‘‘overall activity’’ of AurkB upon Tip60 downregulation, as observed under cancerous conditions.The present work, therefore, uncovers an important functional interplay between AurkB and Tip60, frailty of whichmay be an initial event in carcinogenesis.
Volume 44 | Issue 6
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