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Regeneration of Cardiomyocytes from Bone Marrow Stem Cells and Application to Cell Transplantation Therapy
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Various cardiac specific transcription factors have been cloned, and their genes are serially expressed in the developing heart during myogenesis and morphogenesis. Figure 4 shows the time course of the expression of cardiomyocyte-specific transcription factors in fetal developing heart and CMG cells. The genes coding Nkx2.515 (homeobox type transcription factor specifically expressed beginning in the early developing heart), GATA416 (GATA-motif-binding Zinc finger type transcription factor expressed beginning in the early stage developing heart), HAND 1/2 (basic helix-loop-helix type transcription factor expressed in the heart and autonomic nervous system), and MEF2-B/C17 (muscle enhancement factor: a MADS box family transcription factor expressed in the myocytes) were expressed in the early stage of heart development, and MEF2A and MEF2-D in the middle stage. The CMG cells already expressed GATA4, TEF-118(transcription enhancement factor 2), Nkx2.5, HAND, and MEF2-C before exposure to 5-azacytidine, and they expressed MEF2-A and MEF2-D after exposure to 5-azacytidine. This pattern of gene expression in CMG cells was similar to that of developing cardiomyocytes in vivo,11 and indicated that the developmental stage of the undifferentiated CMG cells is close to that of cardiomyoblasts or the early stages of heart development. We estimated that the stage of differentiation of the CMG cells lies between the cardiomyocyte-progenitor stage and the differentiated cardiomyocyte stage.
Targeting Rho-associated coiled-coil forming protein kinase (ROCK) in cardiovascular fibrosis and stiffening
Published in Expert Opinion on Therapeutic Targets, 2020
Brian Yu, Nikola Sladojevic, John E. Blair, James K. Liao
Serum response factor (SRF), belonging to the MADS box-containing family of transcription factors, is critically involved in fibroblast differentiation, proliferation, and activation [23]. SRF interacts with cofactors from the myocardin-related transcription factor (MRTF) and ternary complex factor (TCF) families, thus coupling growth factor signaling to gene transcription [24]. In particular, MRTF-A and MRTF-B recruitment is crucial for SRF signaling: of the >3100 SRF binding sites identified through chromatin immunoprecipitation sequencing (ChIP-seq), >2600 exhibited MRTF-dependent SRF binding [24]. Indeed, numerous MRTF-SRF-binding sites are located in the promoter regions governing fibroblast activation and inhibition of MRTF/SRF prevents scar tissue formation [25]. The MRTF/SRF pathway is regulated by actin dynamics [20]. For example, G-actin binds to MRTF-A and MRTF-B, sequestering the transcription factor in the cytoplasm (Figure 2). Polymerization of G-actin to F-actin liberates the MRTFs, allowing it to enter the nucleus to associate with SRF and to activate target pro-fibrotic target genes.
Differential expression of flowering genes in Arabidopsis thaliana under chronic and acute ionizing radiation
Published in International Journal of Radiation Biology, 2019
Maryna V. Kryvokhyzha, Konstantin V. Krutovsky, Namik M. Rashydov
To study the effects of irradiation on flowering, we measured the expression of six key flowering-related genes, such as APETALA1 (AP1), CONSTANS (CO), FLOWERING LOCUS C (FLC), FLOWERING LOCUS T (FT), GIGANTEA (GI), and LEAFY (LFY) under irradiation and control condition. The genes CO and GI are regulated by circadian clock and are key genes in the photoperiod flowering time pathway. The FT gene encodes the florigen, a ‘flowering hormone’ or hormone-like protein, responsible for controlling and/or triggering flowering in plants (Smaczniak et al. 2012). The FT gene is expressed also in the vascular tissue of leaves. The FT protein activates the MADS-box genes, important regulators of flower development (Jeong and Clark 2005; Kaufmann et al. 2010).
Multidrug-resistant Candida auris: an epidemiological review
Published in Expert Review of Anti-infective Therapy, 2020
Arunaloke Chakrabarti, Shreya Singh
The role of transporters of the major facilitator MFS and ABC super-families have been reported in C. auris, which play important role in antifungal drug resistance [35]. Apart from these transporters, the acquisition of drug resistance in C. auris is also facilitated by protein kinases and multiple orthologs of zinc cluster transcription factors like TAC1 gene [35,56]. Transcription factors previously known to be involved in the virulence of fungal pathogens such as, the MADS-box and STE related proteins have also been identified in the genome of C. auris [35]. The Ste12p regulates the virulence, cell wall integrity, mating, substrate invasion and filamentation in many fungi while the MADS-box proteins have DNA binding and dimerization activity [57,58]. Additionally, kinases such as Hog1, two-component histidine kinase and protein kinase A (PKA), have been seen in the draft genome of C. auris [35]. While Hog1 protein is implicated in oxidative and hyperosmotic stress response, histidine kinase is critical for morphogenesis and virulence. PKA regulates cellular growth and metabolism in Candida species [59–61]. Compared to C. albicans, higher resistance to cationic, cell wall and oxidative stresses is seen in C. auris [62].Oligonucleotide transporter genes (OPT) in C. auris is implicated in acquisition of nutrient versatility and adaptation to diverse host niches [35,63]. Many known virulence associated genes are conserved in C. auris including mannosyl transferases, which maintain cell wall integrity by coordinating the synthesis of gylcans and play an important role in immune recognition and adherence to host cells [35].