Eppley Institute for Research in Cancer and Allied Diseases

About: Eppley Institute for Research in Cancer and Allied Diseases is a based out in . It is known for research contribution in the topics: Pancreatic cancer & Cancer. The organization has 965 authors who have published 1396 publications receiving 58994 citations.

Improved 3D gd-HCACO and gd-(H)CACO-TOCSY experiments for isotopically enriched proteins dissolved in H2O.

Abstract: Pulsed field gradients were incorporated into the HCACO experiment for acquiring spectra on isotopically enriched protein samples dissolved in H2O. Excellent water suppression and spectral quality were achieved using the modified pulse sequence (gd-HCACO), as demonstrated for a 13C-/15N-labeled sample of the SH2 domain from the hematopoietic cellular kinase dissolved in 90% H2O/10% D2O. Strong correlations for all residues were observed in the gd-HCACO spectrum, even for residues having α-protons resonating exactly at the H2O frequency. The HCACO-TOCSY experiment was modified to correlate intraresidue 13Cα (rather than 1Hα), carbonyl (13C′), and aliphatic side-chain protons [(H)CACO-TOCSY]. Pulsed field gradients were also incorporated into the (H)CACO-TOCSY experiment for water suppression.

Cyclin-dependent kinase 1-mediated AMPK phosphorylation regulates chromosome alignment and mitotic progression

Abstract: AMP-activated protein kinase (AMPK), a heterotrimeric serine/threonine kinase and cellular metabolic sensor, has been found to regulate cell cycle checkpoints in cancer cells in response to energetic stress, to harmonize proliferation with energy availability. Despite AMPK's emergent association with the cell cycle, it still has not been fully delineated how AMPK is regulated by upstream signaling pathways during mitosis. We report, for the first time, direct CDK1 phosphorylation of both the catalytic α1 and α2 subunits, as well as the β1 regulatory subunit, of AMPK in mitosis. We found that AMPK-knockout U2OS osteosarcoma cells have reduced mitotic indexes and that CDK1 phosphorylation-null AMPK is unable to rescue the phenotype, demonstrating a role for CDK1 regulation of mitotic entry through AMPK. Our results also denote a vital role for AMPK in promoting proper chromosomal alignment, as loss of AMPK activity leads to misaligned chromosomes and concomitant metaphase delay. Importantly, AMPK expression and activity was found to be critical for paclitaxel chemosensitivity in breast cancer cells and positively correlated with relapse-free survival in systemically treated breast cancer patients.

Stabilization of a G-Quadruplex from Unfolding by Replication Protein A Using Potassium and the Porphyrin TMPyP4

Abstract: Replication protein A (RPA) plays an essential role in DNA replication by binding and unfolding non-canonical single-stranded DNA (ssDNA) structures Of the six RPA ssDNA binding domains (labeled A-F), RPA-CDE selectively binds a G-quadruplex forming sequence (-TAGGGGAAGGGTTGGAGTGGGTT- called Gq23) In K

Effect of dose on the induction of urothelial proliferation by N -(4-(5-nitro-2-furyl)-2-thiazolyl)formamide and its relationship to bladder carcinogenesis in the rat

Abstract: The effect on urothelial proliferation of a urinary bladder carcinogen, N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT), fed to male F344 rats at doses of 0.2, 0.1, 0.05, 0.01, 0.005 and 0.001% of diet for 4 or 10 weeks was evaluated by autoradiography, using [3H-methyl]thymidine, and by histopathology. At week 4, hyperplasia was induced in 10/11 and 6/11 rats given 0.2% and 0.1% FANFT, respectively. The dose-related increase of labeling index in the bladder epithelium was significant for the groups given 0.01% or higher doses of FANFT. At week 10, histopathologic lesions were observed in groups given 0.05% or higher doses of FANFT. This was accompanied by a significant increase in labeling index for these groups. The results are consistent with the long-term carcinogenicity studies conducted with the same dose levels of FANFT. The interrelationships between numbers of cells (hyperplasia), cell proliferation (labeling index) and cancer induction are discussed utilizing a computerized model of bladder carcinogenesis.