University of Hyderabad

About: University of Hyderabad is a education organization based out in Hyderabad, India. It is known for research contribution in the topics: Catalysis & Crystal structure. The organization has 6446 authors who have published 13005 publications receiving 237641 citations. The organization is also known as: Hyderabad Central University & HCU.

A Mononuclear CoII Coordination Complex Locked in a Confined Space and Acting as an Electrochemical Water‐Oxidation Catalyst: A “Ship‐in‐a‐Bottle” Approach

Abstract: Preparing efficient and robust water oxidation catalyst (WOC) with inexpensive materials remains a crucial challenge in artificial photosynthesis and for renewable energy. Existing heterogeneous WOCs are mostly metal oxides/hydroxides immobilized on solid supports. Herein we report a newly synthesized and structurally characterized metal–organic hybrid compound [{Co3(μ3-OH)(BTB)2(dpe)2} {Co(H2O)4(DMF)2}0.5]n⋅n H2O (Co-WOC-1) as an effective and stable water-oxidation electrocatalyst in an alkaline medium. In the crystal structure of Co-WOC-1, a mononuclear CoII complex {Co(H2O)4(DMF)2}2+ is encapsulated in the void space of a 3D framework structure and this translationally rigid complex cation is responsible for a remarkable electrocatalytic WO activity, with a catalytic turnover frequency (TOF) of 0.05 s−1 at an overpotential of 390 mV (vs. NHE) in 0.1 m KOH along with prolonged stability. This host–guest system can be described as a “ship-in-a-bottle”, and is a new class of heterogeneous WOC.

Role of PI3K-AKT-mTOR and Wnt Signaling Pathways in Transition of G1-S Phase of Cell Cycle in Cancer Cells.

Abstract: The PI3K-Akt pathway together with one of its downstream targets, the mechanistic target of rapamycin (mTOR; also known as the mammalian target of rapamycin) is a highly deregulated pathway in cancers. mTOR exists in two complexes, mTORC1 and mTORC2. Akt phosphorylated at T308 inhibits TSC1/2 complex to activate mTORC1; mTORC2 is recognized as the kinase phosphorylating Akt at S473. Inhibition of autophagy by mTORC1 was shown to rescue disheveled (Dvl) leading to activation of Wnt pathway. Cyclin D1 and the c-Myc are activated by the Wnt signaling. Cyclin D1 is a key player in initiation of cell cycle. c-Myc triggers metabolic reprograming in G1 phase of cell cycle, which also activates the transcription factors like FoxO and p53 that play key roles in promoting the progression of cell cycle. While the role of p53 in cancer cell metabolism in arresting glycolysis and inhibition of pentose phosphate pathway has come to be recognized, there are confusions in the literature on the role of FoxO and that of rictor. FoxO was shown to be the transcription factor of rictor, in addition to the cell cycle inhibitors like p21. Rictor has dual roles; inhibition of c-Myc and constitution of mTORC2, both of which are key factors in the exit of G1-S phase and entry into G2 phase of cell cycle. A model is presented in this article, which suggests that the PI3K-Akt-mTOR and Wnt pathways converge and regulate the progression of cell cycle through G0-G1-S-phases and reprogram the metabolism in cancer cells. This model is different from the conventional method of looking at individual pathways triggering the cell cycle.