Examinando por Autor "Aroca Martinez, Gustavo"
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Ítem Cell Signaling in Neuronal Stem Cells(MDPI, 2018-07) Navarro Quiroz, Elkin; Navarro Quiroz, Roberto; Ahmad, Mostapha; Gomez Escorcia, Lorena; Villarreal, Jose Luis; Fernandez Ponce, Cecilia; Aroca Martinez, GustavoThe defining characteristic of neural stem cells (NSCs) is their ability to multiply through symmetric divisions and proliferation, and differentiation by asymmetric divisions, thus giving rise to different types of cells of the central nervous system (CNS). A strict temporal space control of the NSC differentiation is necessary, because its alterations are associated with neurological dysfunctions and, in some cases, death. This work reviews the current state of the molecular mechanisms that regulate the transcription in NSCs, organized according to whether the origin of the stimulus that triggers the molecular cascade in the CNS is internal (intrinsic factors) or whether it is the result of the microenvironment that surrounds the CNS (extrinsic factors).Ítem Epigenetic mechanisms and posttranslational modifications in systemic Lupus Erythematosus(Multidisciplinary Digital Publishing Institute (MDPI), 2019) Navarro Quiroz, Elkin; Chavez-Estrada, Valeria; Macias-Ochoa, Karime; Ayala-Navarro, María Fernanda; Flores-Aguilar, Aniyensy Sarai; Morales-Navarrete, Francisco; De la Cruz Lopez, Fernando; Gomez Escorcia, Lorena; G. Musso, Carlos; Aroca Martinez, Gustavo; Gonzales Torres, Henry; Diaz Perez, Anderson; Cadena Bonfanti, Andres; Sarmiento Gutierrez, Joany; Meza, Jainy; Diaz Arroyo, Esperanza; Bello Lemus, Yesit; Ahmad, Mostapha; Navarro Quiroz, RobertoThe complex physiology of eukaryotic cells is regulated through numerous mechanisms, including epigenetic changes and posttranslational modifications. The wide-ranging diversity of these mechanisms constitutes a way of dynamic regulation of the functionality of proteins, their activity, and their subcellular localization as well as modulation of the di erential expression of genes in response to external and internal stimuli that allow an organism to respond or adapt to accordingly. However, alterations in these mechanisms have been evidenced in several autoimmune diseases, including systemic lupus erythematosus (SLE). The present review aims to provide an approach to the current knowledge of the implications of these mechanisms in SLE pathophysiology.Ítem Lymphoid peritoneal fluid as a variant of chylous-like effluent in peritoneal dialysis: proposal for a new diagnostic term(Società Italiana di Nefrologia, 2024) Fernández Claros, Nigel; Ocampo, María L.; Musso, Carlos G.; Cristiano, Fabrizio; Aroca Martinez, Gustavo; Giordani, María C.The cloudy bag in peritoneal dialysis is generally associated with infectious peritonitis and non-infectious etiologies. These cloudy bags may have increased cellularity or low/acellular counts. In the case of low cell count, the concomitant detection of fibrin or fat can provide guidance on its etiology. The cloudy peritoneal bag with a whitish appearance is usually due to its high fat content (chyloperitoneum). The etiologies include pharmacological, traumatic or inflammatory causes. The elevated fatty component in chyloperitoneum may be triglycerides (chylous), cholesterol (pseudochylous) or lymph. We present the case of a patient with stage 5 chronic kidney disease (CKD). He starts continuous ambulatory peritoneal dialysis and presents turbid but acellular peritoneal effluent with chylous appearance, negative cultures, and low levels of triglycerides and cholesterol on physicochemical evaluation. It doesn’t meet the criteria for chylous or pseudochylous fluid, which is why the term lymphoid fluid is here proposed to describe it, because of its resemblance to lymphatic fluid in color. To our knowledge, this is the first case in the literature to report this effluent (milky-looking fluid without high levels of triglycerides or cholesterol) and to propose a specific term to describe it.Ítem The role of glycosyltransferases in colorectal cancer(MDPI, 2021) Fernández-Ponce, Cecilia; Geribaldi-Doldán, Noelia; Sánchez-Gomar, Ismael; Navarro Quiroz, Roberto; Atencio Ibarra, Linda; Gomez Escorcia, Lorena; Fernández-Cisnal, Ricardo; Aroca Martinez, Gustavo; García-Cózar, Francisco; Navarro Quiroz, ElkinColorectal cancer (CRC) is one of the main causes of cancer death in the world. Post-translational modifications (PTMs) have been extensively studied in malignancies due to its relevance in tumor pathogenesis and therapy. This review is focused on the dysregulation of glycosyltransferase expression in CRC and its impact in cell function and in several biological pathways associated with CRC pathogenesis, prognosis and therapeutic approaches. Glycan structures act as interface molecules between cells and their environment and in several cases facilitate molecule function. CRC tissue shows alterations in glycan structures decorating molecules, such as annexin-1, mucins, heat shock protein 90 (Hsp90), β1 integrin, carcinoembryonic antigen (CEA), epidermal growth factor receptor (EGFR), insulin-like growth factor-binding protein 3 (IGFBP3), transforming growth factor beta (TGF-β) receptors, Fas (CD95), PD-L1, decorin, sorbin and SH3 domain-containing protein 1 (SORBS1), CD147 and glycosphingolipids. All of these are described as key molecules in oncogenesis and metastasis. Therefore, glycosylation in CRC can affect cell migration, cell–cell adhesion, actin polymerization, mitosis, cell membrane repair, apoptosis, cell differentiation, stemness regulation, intestinal mucosal barrier integrity, immune system regulation, T cell polarization and gut microbiota composition; all such functions are associated with the prognosis and evolution of the disease. According to these findings, multiple strategies have been evaluated to alter oligosaccharide processing and to modify glycoconjugate structures in order to control CRC progression and prevent metastasis. Additionally, immunotherapy approaches have contemplated the use of neoantigens, generated by altered glycosylation, as targets for tumor-specific T cells or engineered CAR (Chimeric antigen receptors) T cells.