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Insulinoma
Published in Demetrius Pertsemlidis, William B. Inabnet III, Michel Gagner, Endocrine Surgery, 2017
In a meta-analysis of 6222 cases, 87.1% of insulinomas were benign [17], and they have a good survival. Five-year survival rates are reported to be 60%–100%. The cause of insulinoma has for a long time been obscure. Studies in rats, however, have shown that the chemokine (C-X-C motif) ligand 12 (CXCL12) is a pre-beta-cell growth-stimulating factor [18, 19], and overexpression of this gene leads to resistance to apoptosis, and consequently lack of diabetes [20]. Yin Yang 1 (YY1) is a ubiquitous zinc-finger transcription factor that regulates transcription [21], and studies have shown that YY1 strongly activates transcription of CXCL12 [22]. Mutations in YY1 are demonstrated at T372R in the third functional zinc-finger domain in YY1 responsible for transcriptional repression [23, 24], implying an activation of the transcription of genes specific for leading to increased insulin secretion and beta-cell proliferation (ADCY1 and CACNAD2D2), and subsequently to insulinoma formation. The mutation was found in approximately 30% of investigated insulinomas. Other reports demonstrate a gain at chromosome locus 9q34 in insulinomas [25].
Adenoviruses
Published in Dongyou Liu, Laboratory Models for Foodborne Infections, 2017
Anthony P. Malanoski, Baochuan Lin
The majority of nonstructural proteins of AdVs are encoded by the early-transcribed genes. E1A is the first gene expressed upon viral infection and plays an essential role in regulating the viral transcription of genes necessary for replication and reprograming the cellular transcription to facilitate viral replication. Two major E1A proteins, 12S and 13S E1A, are synthesized via alternative splicing of mRNA transcripts, which results in a 46 aa conserved region (CR3) that is unique in 13S E1A. Despite their similarity, 13S E1A is primarily responsible for activating the viral gene expression via CR3, while 12S E1A represses transcription, which is achieved via temporal regulation.79–82 E1A proteins activate transcription through a TATA motif, YY1 recognition sites, by interacting with a variety of cellular transcription factors and relieving transcription repression.2 In addition to modulating transcription, E1A proteins also regulate signaling pathways and 26S proteasome, interfere with pathways involved in immune regulation, as well as involve the evasion of T-cell immunity to ensure viral survival and infectivity.82
Vitamin C Alimentation via SLC Solute Carriers
Published in Qi Chen, Margreet C.M. Vissers, Vitamin C, 2020
Damian Nydegger, Gergely Gyimesi, Matthias A. Hediger
The substrate ascorbic acid of SVCT1 and SVCT2 is an important regulator for these transporters. In Gulo−/− mice, which depend on ascorbic acid uptake from the diet, ascorbic acid starvation led to increased mRNA and protein expression of SVCT1 and SVCT2 in the liver, increased expression of SVCT2 in the cerebellum, and increased expression of SVCT1 in the small intestine. Also during development in mice, expression levels and ascorbic acid levels change. In late embryonic and early natal stages, the cortex and cerebellum of these mice have high ascorbic acid levels and low SVCT2 mRNA and protein levels. During adolescence, the expression of SVCT2 mRNA and protein is increased, and the ascorbic acid levels decrease. A development in a similar direction occurs in the liver of the mice: at birth, the expression levels of SVCT1 and SVCT2 are low, increasing over time [2]. It was shown that the hepatocyte nuclear transcription factor HNF1α (hepatocyte nuclear factor 1 homeobox alpha) increases the SVCT1 promotor activity (Figure 3.4) [4,59,60]. HNF1α transcription is inhibited when the NF-κB (nuclear factor–kappa light chain enhancer of activated B cells) signaling pathway is activated. The activated NF-κB pathway leads to increased levels of inflammatory cytokines and cell death [4]. SVCT2 is also regulated in the same manner by HNF1α. SVCT1 and SVCT2 are both regulated on the transcriptional level by transcription factor Sp1. A decrease in Sp1 leads to decreased mRNA and protein levels of SVCT1 and SVCT2 [60]. Other transcription factors such as SP3 and YY1 are also reported to regulate the expression of these transporters [61]. The euchromatin markers H3K4me3 [62,63] and H3K9ac also increase the expression of SVCT1 and SVCT2 [62]. The expression of SVCT1 and SVCT2 depends on many factors, and it is currently an active research topic because of their important role in vitamin C homeostasis.
Yin Yang 1 impacts upon preeclampsia by regulating Treg/TH17 cells and PI3K/AKT pathway
Published in Journal of Immunotoxicology, 2023
Haowen Li, Ling Yu, Yiling Ding, Yanting Nie, Mengyuan Yang
Yin Yang 1 (YY1) is a transcription factor that interacts with different regulatory proteins such as transcription factors, co-activators, and co-repressors (Castellano et al. 2009). YY1 has pleiotropic effects on multiple cellular processes, including cell growth, apoptosis, and differenti- ation (Gordon et al. 2006). With respect to cells/processes associated with PE, YY1 was shown to regulate trophoblast-endothelial cell interaction network under the regulation of miR-651-3p (Yin et al. 2021). Evidence has also shown that YY1 can affect the proliferation and infiltration of trophoblasts by regulating cytoskeleton-related proteins (Tian et al. 2016). With regard to the immune system, Hwang et al. (2016) reported YY1 could suppress the differentiation and subsequent functionality of Treg cells in part by blocking expression of forkhead box P3 (Foxp3) and its target genes. Apart from what the above studies suggest, there is still no direct evidence to support a potential role for YY1 in regulating the onset/progression of PE.
Dietary betaine prevents obesity through gut microbiota-drived microRNA-378a family
Published in Gut Microbes, 2021
Jingjing Du, Peiwen Zhang, Jiang Luo, Linyuan Shen, Shunhua Zhang, Hao Gu, Jin He, Linghui Wang, Xue Zhao, Mailing Gan, Liu Yang, Lili Niu, Ye Zhao, Qianzi Tang, Guoqing Tang, Dongmei Jiang, Yanzhi Jiang, Mingzhou Li, Anan Jiang, Long Jin, Jideng Ma, Surong Shuai, Lin Bai, Jinyong Wang, Bo Zeng, De Wu, Xuewei Li, Li Zhu
miRNAs are known to modulate biological processes through base pairing with the 3′-untranslated regions (3′UTR) of the target mRNAs.58 Among these potential target genes of miR-378a family, Yin Yang 1 (YY1) was regulated by gut microbiota and showed an expression pattern opposite to that of the miR-378a family (Supplementary Figure 13A-J). To identify whether betaine-derived gut microbiota/miR-378a family improved obesity through YY1, we first examined the link between YY1 and miR-378a family. As expected, the expression of YY1 could be negatively regulated by the miR-378a family (Supplementary Figure 13 K-M). Overexpression of miR-378a family significantly repressed YY1 activity by binding to their 3′-UTR (Figure 4c), suggesting that YY1 was a direct target gene of miR-378a family. Supporting previous findings that YY1 contributes to HFD-induced obesity,65–68 improvement in lipid metabolism (Figure 4d-e) and glucose homeostasis (Figure 4f) by betaine or miR-378a family was obviously reduced by increasing YY1. Furthermore, increasing YY1 almost abolished betaine- or miR-378a family-mediated lipogenesis inhibition (Figure 4g), BAT inactivation (Figure 4h), and browning of iWAT (Figure 4i, j) in HFD-fed mice. These results therefore implicate that YY1 as an important player for improvement of obesity and MS by betaine-derived gut microbiota/miR-378a family.
Expression of YY1 in pro-B and T phenotypes correlation with poor survival in pediatric acute lymphoblastic leukemia
Published in Pediatric Hematology and Oncology, 2021
Gabriela Antonio-Andres, Elva Jiménez-Hernandez, Laura A. Estrada-Abreo, Yanelly Garfias-Gómez, Genaro Patino-Lopez, Sergio Juarez-Mendez, Sara Huerta-Yepez
On the other hand, YY1 has been suggested to be a critical factor in T cells, both in their normal differentiation and induction of T cell-mediated diseases. YY1 is involved in the thymus development of CD4 and CD8 T cells, the various subsets of CD4, Th1, Th2, Th17, and Treg. In addition to being necessary for the maturation and proliferation of the lineage through its role in the mediation of the apoptotic pathway, it controls the expression of the Th2 master regulator GATA3. YY1 cooperates with GATA3 and is necessary for the regulation of the Locus of Th2 cytokines.22 All the evidence mentioned above demonstrates that YY1 plays and important role in the differentiation of pro-B cell to pre-B and also in the differentiation of T cells.