2058 research outputs found
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Woollins Reagent: A Chemoselective Reducing Agent for 1,4-Enediones and 1,4-Ynediones to Saturated 1,4-Diones
No full textWoollins reagent was found to act as a highly chemoselective
reagent for the reduction of a wide range of 1,4-enediones
and 1,4-ynediones in methanol to afford the corresponding saturated 1,4-diketones in good yields under mild reaction conditions
Synthesis of S-thiomethyl MAG3, radiolabelling with technetium-99m and biological evaluation
No full textProtection of the thiolate function of the mercaptoacetyltriglycine (MAG3) by S-thiomethyl group allows automatic deprotection of the protecting group during technetium-99m radiolabelling by transchelation using stannous chloride dihydrate as reductant. Protection of the thiolate group with S-thiomethyl increases the stability of the ligand, desired complex of high
radiochemical purity could be prepared under relatively mild labelling condition (at room temperature) omitting the aeration step. The complex prepared from the S-thiomethyl protected MAG3 ligand were chromatographically (HPLC) and biologically compared with the corresponding complex prepared from the S-benzoylated MAG3 precursor. This result suggests that technetium-99m complex of MAG3 could be prepared from S-thiomethylated MAG3 precursor in comparatively higher purity under relatively milder labelling condition and this method of radiolabelling could be used for the development of less cumbrous single vial MAG3 ki
ETS-1 Protein Regulates Vascular Endothelial Growth Factor-induced Matrix Metalloproteinase-9 and Matrix Metalloproteinase-13 Expression in Human Ovarian Carcinoma Cell Line SKOV-3
No full textThe mechanism of vascular endothelial growth factor (VEGF)-regulated expression of MMPs followed by
cancer cell scattering/invasion is poorly understood.
VEGF induces MMP-9, MMP-13, and ETS-1 through PI3K/AKT and p38 MAPK pathways in SKOV-3 cells.
VEGF induces ETS-1, which activates specific MMPS, leading to the invasion/scattering in SKOV-3 cells.
This study provides useful information that reveals the molecular mechanism of ovarian cancer metastasis
Au(I)- and Pt(II)-N-heterocyclic carbene complexes with picoline functionalized benzimidazolin-2-ylidene ligands; synthesis, structures,electrochemistry and cytotoxicity studies
No full textNovel Au(I)-N-heterocyclic carbene complexes, 1-methyl-3-(2-pyridylmethyl)-
benzimidazolylidenegold(I)-chloride, 1; 1-benzyl-3-(2-pyridylmethyl)-
benzimidazolylidenegold(I)chloride, 2; and Pt(II)-N-heterocyclic carbene complexes 1-methyl-3-(2-
pyridylmethyl) benzimidazolylidene platinum(II)chloride, 3; and 1-benzyl-3-(2-pyridylmethyl)
benzimidazolylidene platinum-(II)chloride, 4, have been synthesized, based on CN-donor proligands
1-alkyl-3-(2-pyridylmeth-yl)-benzimidazoliumchloride L1 and L2 [alkyl, R = –CH3 = L1;
R = –CH2Ph = L2]. All the compounds have been synthesized and characterized by different
spectroscopic methods. The Au(I) complexes 1 and 2 have been synthesized by a silver carbene
transfer method. The solid-state structures of 1 and 3 have been determined by single crystal
X-ray diffraction studies. The square planar Pt(II) complexes 3 and 4 show a reversible
Pt(II)/Pt(IV) couple at 0.69 eV and 0.67 eV respectively. Among the complexes 1–4, complexes 1
and 3 have been used for cytotoxicity studies on the cell lines B16F10 (mouse melanoma), HepG2
(human hepatocarcinoma) and HeLa (human cervical carcinoma). IC50 values are compared with
cisplatin, among 1 and 3, the Au(I) complex 1 is more effective than Pt(II) complex 3
Expedient and Facile One-Pot Syntheses of Triazole-Linked Glycoconjugates under Microwave Irradiation
No full textEffective microwave assisted one-pot syntheses of triazole-
O-glycoconjugates and triazolylglycosides involving sequential
glycosylation and click chemistry are described
Multimeric Proteins: Its Adaptation and Regulation of Biological Activities
No full textProteins are one of the major structural and functional components of all living systems. The word protein is derived from the Greek word prôtos, meaning primary or first rank of importance and with good reason. More than half the dry weight of a cell is made up of proteins. They virtually control directly and indirectly all cellular functions. Each protein within the body is involved for a single or multiple specific functions. Some proteins are
involved exclusively in structural support, while others are involved in bodily movement or defense against germs etc. Different structures of proteins define different functions. They may be round, globular shape (like hemoglobin whose spherical shape is useful for maneuvering through blood vessels), long (like collagen, whose stringy, strong rope like structure provides great support),
strong (like spectrin c which protects erythrocytes from the powerful shearing forces they are exposed to) or elastic (like titin which controls muscle stretching and contraction)
Corchorusin-D Directed Apoptosis of K562 Cells Occurs through Activationof Mitochondrial and Death Receptor Pathways and Suppression of AKT/PKB Pathway
No full textSaponins, plant glycosides, have been reported to possess anti-cancer properties. Therefore
the effect of corchorusin-D (COR-D), a compound isolated from Corchorus acutangulus, was
studied in the chronic myelogenous leukemic cell line K562, using MTT assay, phase contrast
and confocal microscopy, annexin V binding, cell cycle analysis and western blotting. COR-D
inhibited cell growth in K562 cells and showed increased number of Annexin V FITC binding
cells. Characteristic apoptotic changes, seen under phase contrast and confocal microscopes
with accumulation of cells in the sub-G0 phase. The apoptosis involved drop in Bcl-2/Bax
ratio, loss of mitochondrial membrane potential, release of cytochrome c in cytosol followed
by activation of caspases 9 and 3, and cleavage of PARP. Down-regulation of pro-caspase 10
was observed along with formation of death-inducing signaling complex between TNF-R1
and TRADD. COR-D suppressed PDK1 and AKT with activation of MAP kinase family members
ERK1/2, JNK1/2 and p38. Thus it induced apoptosis by activating mitochondrial and death
receptor pathways and suppressing AKT/PKB rather than MAP kinase pathway. Significant
enhancement of apoptosis, noted using specific inhibitors of ERK1/2, p38 and JNK1/2, suggests
that COR-D can enhance apoptosis in K562 cells in combination with MAP kinase inhibitors
Studies on the Structural and Energetic Aspects of the Interaction of Phenazinium Dyes with Deoxyribonucleic Acids
No full textNucleic acids are the central molecules in transmission, expression and conservation of genetic information.
Nucleic acids were first discovered by Friedrich Miescher in 1871. This Swiss physician and biologist isolated
various phosphate-rich chemicals, which he called nuclein (now nucleic acids), from the nucleic acids of
white blood cells in 1869.
After Miescher’s initial description in 1871, other scientists also started investigations into
nuclein. However, for long after Miescher’s death, nuclein still received comparatively little attention. The
role of DNA as the carrier of genetic information has been amply demonstrated beginning with the classic
experiments of Avery1and Hershey and Chase2. Identifying DNA as the code of life was a remarkable discovery.
However, uncovering the structure of DNA would prove to be the key to understand the role it plays in
the formation of life. This structure has novel features which are of considerable biological interest. The classic
example of how biological functions follow from biomolecular structures comes from the elucidation of the
structure of DNA as a double helix by Watson and Crick3 using the X-ray fiber diffraction patterns
generated by Franklin, Wilkins, and their associates.4,5 “We wish to suggest a structure for the salt of
deoxyribonucleic acid (DNA)” –this was the opening remark in the paper published in the Nature magazine
by Watson and Crick announcing discovery of the structure of DNA in the year 1953. This discovery is often
said to mark the birth of modern molecular biology
In situ Reversible Aggregation of Extracellular Cellobiase in the Filamentous Fungus Termitomyces clypeatus
No full textCellobiase (E.C. 3.2.1.21), is a widely exploited
industrial glycosidase with a major role in biofuel industry.
Its stability and shelf life are major bottlenecks in
achieving a superior formulation for industry. In the
filamentous fungus Termitomyces clypeatus, the enzyme is
secreted in a co-aggregated form with sucrase; the
separation of this co-aggregation results in substantial loss
of the enzyme’s activity. The aim of the present study was
to examine the mode of aggregation of the secreted
cellobiase-sucrase coaggregate and its role in the
stabilization of cellobiase. Transmission electron microscopy
and dynamic light scattering of purified co-aggregates
revealed reversible, concentration driven self-aggregation
of the extracellular enzymes to form larger entities.
However, the intracellular enzyme aggregates were rigid,
non-interacting, and possessed a higher percentage of
disulphide bonds. Circular dichroic spectra of the two coaggregates
indicated no significant difference in secondary
structures. Self-association increased the stability of
extracellular aggregates towards heat by 1.5 fold, SDS by
4 ~ 7 fold, and chaotropic agents, by 1.5 ~ 2 fold, than the
intracellular counterpart. The Km of extracellular aggregate
varied between 0.29 and 0.45 mM as a result of
spontaneous aggregation and disaggregation, whereas that
of intracellular aggregate was 0.22 mM irrespective of its
concentration status. In situ detection of cellobiase in
native PAGE revealed two activity bands of the
extracellular enzyme, which indicated a minimum of two
active dissociated aggregate species, as compared to a
single band for the intracellular enzyme. These studies are
believed to improve the understanding of aggregation of
the fungal glycosidases, which remains to be a blackbox, to
increase the efficacy of these enzyme
Elucidation of the Signaling Mechanisms Involved in the Subversion of Host Immune Response by Intracellular Parasite Leishmania Donovani
No full textThe intracellular parasite L. donovani has the unique capacity to survive and replicate inside host macrophages. Since this cell type is specialized for the destruction of invading pathogens and priming of the host immune response, Leishmania has had to evolve a range of sophisticated mechanisms to subvert normal macrophage function. This enables the parasite to evade the innate immune response and to divide within the phagolysosome of the infected
macrophage, from where it can spread and propagate the disease within the host. There are multiple ways by which intracellular pathogens like Leishmania make use of host cell’s machinery in order to survive and replicate. One such mechanism is the distortion of host macrophage’s own signaling pathways to selectively repress or enhance the expression of various cytokines and microbicidal molecules and antigen presentation. Within the scope of
this work, an attempt has been made to focus on the molecular mechanisms by which Leishmania can subvert host immune surveillance by altering the macrophage signal
transduction machinery, thereby modulating the macrophage environment in its favour.
Toll-like receptors (TLRs), which form an interface between mammalian host and microbe, play a key role in pathogen recognition and initiation of pro-inflammatory response thus
stimulating antimicrobial activity and host survival. However, certain intracellular pathogens like Leishmania, can successfully manipulate the TLR signaling, thus hijacking the defensive strategies of the host. Despite the presence of lipophosphoglycan (LPG), a TLR2 ligand
capable of eliciting host-defensive cytokine response, on the surface of Leishmania, the strategies adopted by the parasite to silence the TLR2-mediated pro-inflammatory response is not understood. Although the ability of Leishmania to inhibit inflammatory signaling
pathways has been proposed as a virulence mechanism, the molecular events underlying this process remain still to be explored. The aim of this study was to determine the mechanism used by Leishmania to modulate TLR signaling cascade for its own favor