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Effects of Retinoids at the Cellular Level (Differentiation, Apoptosis, Autophagy, Cell Cycle Regulation, and Senescence)
Published in Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish, Retinoids in Dermatology, 2019
The entry of RA into the nucleus, where binding to receptors occurs, depends upon the retinoid binding proteins. These cytosolic proteins include cellular retinol-binding proteins (RBP): RBP1, RBP2, cellular retinoic acid-binding protein 1 and 2 (CRABP1, CRABP2), and fatty acid-binding protein 5 (FABP5), which are responsible for cellular transport of poorly soluble retinoids during uptake, metabolism, and function (5).
From a basic to a functional approach for developing a blood stage vaccine against Plasmodium vivax
Published in Expert Review of Vaccines, 2020
Manuel Alfonso Patarroyo, Gabriela Arévalo-Pinzón, Darwin A. Moreno-Pérez
Attempts have thus been made to determine various P. vivax molecules’ immunogenicity and antigenicity. Although the parallel study of the immune response’s contribution against various antigens was expensive and slow over 9 years ago, the arrival of the postgenomic era has rapidly led to discovering a large panel of P. vivax Mrz immunoreactive molecules [33–35]. In silico prediction and cell-free expression systems coupled to protein array systems have been used for processing sera from populations naturally exposed to the parasite. Prospective studies have used such methodology, suggesting that some Abs which are specific against known P. vivax proteins such as PvEBP, PvCyRPA, PvMSP3α, PvRBP2b, PvRBP1a, Pv41, PvRhopH2, PvDBP1 region II (DBP1-RII), PvRBP2-P2, PvMSP9, Pv12, PvAMA1, PvRBP2c, and PvRBP2a are associated with a reduced risk of clinical disease [36–40].
Combination of podophyllotoxin and rutin modulate radiation-induced alterations of jejunal proteome in mice
Published in International Journal of Radiation Biology, 2020
Sania Bajaj, Syed Imteyaz Alam, Basir Ahmad, Humaira Farooqi, Manju Lata Gupta
Together, the previous reports and the current proteomic study have indicated a positive modulatory role of G-003M over a vast network of biomolecular moieties like enzymes, signaling molecules, transcription factors, etc. This has helped in providing protection and restoration of GI tissue morphology and homeostasis (retinol-binding protein 2) by repairing the damage and boosting endogenous machinery (Aldh2; Txndc 17) to face effect of radiation. Based on previous but also current findings, our formulation G-003M is under study in large animal model (non-human primates) for its protective role against radiation. On getting favorable results, this formulation may further be promoted for its regulated clinical trial studies for human application.
Molecular insights into cancer drug resistance from a proteomics perspective
Published in Expert Review of Proteomics, 2019
Yao An, Li Zhou, Zhao Huang, Edouard C. Nice, Haiyuan Zhang, Canhua Huang
Following protein expression by the gene, most proteins must be modified by covalent addition of various functional groups such as glycosylation, phosphorylation, methylation or ubiquitination to gain complete function. At present, more than 300 different kinds of protein PTMs have been identified, many of which are deemed to have important roles in numerous biological and pathological processes [118]. PTMs have been proposed to have a great effect on cancer drug resistance [119]. It is important to highlight the role of PTMs on histones, basic proteins which interact with DNA to form the nucleosome, the fundamental repeating unit of chromatin [120]. The packaging of histones with DNA regulates the chromatin state, which is known to contribute to the control of gene expression. PTMs on histones include methylation, acetylation, phosphorylation and ubiquitylation, which are thought to contribute to the control of gene expression by influencing chromatin compaction or recognition by specific proteins [121]. PTMs on proteins in resistant cancer are distinct from those found in sensitive cancers. Enhancer of zeste homolog 2 (EZH2) is a histone methyltransferase mediating di- and tri-methylation of histone H3 at lysine 27 (H3K27me2/3), leading to transcriptional silencing of specific genes. Recent studies suggest that loss of EZH2 induces resistance to multiple drugs in acute myeloid leukemia [122]. Retinoblastoma-binding protein 2 (RBP2, also known as KDM5A) is a demethylase which di- and tri-methylates histone H3 at lysine 4 (H3K4me2/3). Knockdown of RBP2 induced tamoxifen sensitivity, while overexpression of RBP2 conferred tamoxifen resistance in vitro and in vivo in breast cancer [123]. MS-based proteomics is able to decipher a plethora of PTMs that may contribute to potential biomarker discovery and drug target development. The use of top down methodologies, which are proving effective in the analysis of PTMs, will further assist such studies [124].