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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).
Plasma Cell Neoplasms
Published in Tariq I. Mughal, Precision Haematological Cancer Medicine, 2018
The term ‘smouldering multiple myeloma’ (SMM), also known as ‘smouldering’, indolent or asymptomatic myeloma, coined by the Mayo Myeloma Group (Minnesota), and is a precursor phase of active myeloma. At diagnosis, all patients are asymptomatic, and the term was introduced to help identify patients who have a higher risk of progressing to symptomatic MM, compared with MGUS. A principal challenge in the management of patients with SMM is the precise timing of treatment initiation. Genetic studies suggest an incremental genetic complexity as the disease evolves from a precursor state to symptomatic MM, but the precise molecular mechanisms leading to this progression remain an enigma. Mutations in BRCA2 and UNC5D have been observed in SMM, but not in symptomatic MM; methylation of the genes, GPX3, RBP1, SPARC and TGFB1, which play a role in immunomodulation of the bone marrow microenvironment, have also been noted. Clinically, SMM is arbitrarily distinguished from MGUS by the presence of >10%, and <60%, clonal bone marrow plasma cells, a monoclonal immunoglobulin (M-protein) level >30 g/L or both. The initial rate of SMM progressing to symptomatic MM is about 10% per annum in the first 5 years, then decreases to about 3% per annum for the next 5 years and thereafter approaches the transformation risks of MGUS, about 1% per annum.
All-Trans Retinoic Acid Prevents the Progression of Gastric Precancerous Lesions by Regulating Disordered Retinoic Acid Metabolism
Published in Nutrition and Cancer, 2022
Hanhan Wu, Didi Zhao, Chen Wang, Daoming Zhang, Min Tang, Shiqing Qian, Lina Xu, Tao Xia, Juanyan Zhou, Guangjun Wang, Yue He, Lei Gao, Wenjun Chen, Li Li, Wanshui Yang, Qihong Zhao, Chuanlai Hu, Anla Hu
Among the 68 local patients diagnosed with gastric lesions, there were no significant differences in any of the demographic characteristics (Table 1). First, we comprehensively detected the mRNA expression involved in the synthesis (STRA6, RBP1, RBP4, BCO1, LRAT, RDH10, ALDH1A1, and ALDH1A2), transport (CRABP1 and CRABP2), and decomposition (CYP26A1, CYP26B1, and CYP26C1) of RA metabolism by qRT–PCR in the gastric mucosa. As shown in Figure 2(A) and Supplementary Figure S1, no significant differences were found in mRNA levels among these factors, except RDH10, ALDH1A1, and CYP26B1 between NAG, GPL, and GC patients. The mRNA levels of RDH10, ALDH1A1, and CYP26B1 varied significantly in GC cases (P<0.05) but not between NAG and GPL cases. The results of Figure 2(B,C) suggested that with the aggravation of gastric lesions, the protein expression of RA anabolic enzymes (RDH10 and ALDH1A1) decreased, while the expression of the catabolic enzyme (CYP26B1) was upregulated, although the differences between NAG and GPL were not statistically significant. The corresponding hematoxylin and eosin staining of immunohistochemical cases in Figure 2(C) was shown in Supplementary Figure S2, where the gastric tissue structure of different gastric lesions was well displayed.
Inhaled multi-walled carbon nanotubes differently modulate global gene and protein expression in rat lungs
Published in Nanotoxicology, 2021
Carole Seidel, Vadim Zhernovkov, Hilary Cassidy, Boris Kholodenko, David Matallanas, Frédéric Cosnier, Laurent Gaté
The direct comparison of DEGs and DEPs revealed small amounts of overlapping genes and proteins. Figure 1(C) summarizes the numbers of genes and proteins that were differentially expressed and represents genes and proteins that were found to be simultaneously differentially expressed. The maximum number of overlapped genes and proteins was found for the high dose of NM-401 on day 3, while the maximum percentage of the overlapping pairs was identified for a later time: the values were doubled. On day 3 after exposure to the high dose of NM-401, 22 genes/proteins were simultaneously differentially expressed: Azgp1, C1qa, C4bpa, Cfb, Cotl1, Ctsh, Ctss, Dcps, Dnaja4, Fabp4, Fdps, Fgl2, Gpnmb, Hnrnpdl, Hspa5, Hspd1, Lpl, Mb, Pdia6, Rbp1, Sftpd, Spp1. On day 180 after exposure to a high dose of NM-403, 9 genes/proteins were simultaneously differentially expressed: Agt, Enpp2, Fabp5, Itih1, Lcn2, Lgals3, Lpo, RT1-Bb, Vnn3.
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
The first P. vivax protein–cell interaction studies date back to experiments with complete PvRBP1 and 2 molecules [96] (currently called PvRBP1a and PvRBP2c [97]) and PvDBP1 protein [28,98] or their fragments. Access to samples from a patient having high reticulocyte concentration (~85%) led to the fine mapping and identification of PvDBP1, PvRBP1a and PvMSP1 cHABPs [41] (Figure 1). Promising results were obtained in trials which involved immunizing Aotus nancymaae monkeys with recombinant polypeptides containing binding regions from the 33 kDa PvMSP1 fragment (i.e. rPvMSP114 and rPvMSP120) [41]. This resulted in 4/12 monkeys experimentally challenged with a P. vivax heterologous strain becoming partially protected and 2 totally so. A later study provided partial protection in four out of five monkeys, using the same immunization protocol but with three doses.