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Regulation of Growth of Airway Smooth Muscle by Second Messenger Systems
Published in Alastair G. Stewart, AIRWAY WALL REMODELLING in ASTHMA, 2020
New insights into the mechanisms by which cAMP-dependent pathways inhibit cell growth have recently been described. The activation of A-kinase results in the inhibition of Raf-1 activation in mammalian cells.98,99 Raf-1, a serine/threonine protein kinase, is an effector for Ras-GTP, and the interaction of Raf-1 with Ras-GTP induces Raf activation. Activation of Raf-1 phosphorylates and activates other serine/threonine kinases, which ultimately activates the mitogen-activated protein kinase (MAPK) pathway. This pathway is thought to be critically important in modulating mitogen-induced cell proliferation of some cell types.
Short-Term Exercise and Immune Function
Published in Ronald R. Watson, Marianne Eisinger, Exercise and Disease, 2020
The morphological transformation of T-lymphocytes to blast cells has been observed during the induction of graft vs. host disease and during the sensitization of normal guinea pigs to chemical allergens.27 Thus, lymphocytes are transformed morphologically and functionally in response to antigenic stimulation. The fact that lymphocytes can be transformed in vitro by specific antigens or many nonspecific mitogens provides a useful system for studying mechanisms of immunoregulation and control in mammalian cells. Mitogen-induced cell proliferation is a useful, in vitro, diagnostic measure of cell- mediated immune function.29 The in vitro proliferative response of lymphocytes when cultured in the presence of mitogens and antigens is generally agreed to reflect global in vivo immunological function.27
Apoptosis: Cellular Signaling and Molecular Mechanisms
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
Rosemary B. Evans, John A. Cidlowski
Expression of many proto-oncogenes is required for the mitogenic response and for normal progression of the cell cycle. Mitogen deprivation of cells frequently leads to apoptosis.2 Thus, it is reasonable to believe that genes involved in regulation of cellular proliferation may also be involved in regulation of programmed cell death. This hypothesis is supported by the observation that the expression of several proto-oncogenes (c-myc, c-myb, c-Ki-ras) involved in cell cycle regulation is decreased in glucocorticoid-treated lymphoid cells undergoing apoptosis.2
RBD- specific Th1 responses are associated with vaccine-induced protection against SARS-CoV-2 infection in patients with hematological malignancies
Published in OncoImmunology, 2023
Camille Bigenwald, Yacine Haddad, Cassandra Thelemaque, Agathe Carrier, Roxanne Birebent, Pierre Ly, Caroline Flament, Imran Lahmar, Eric de Sousa, Markus Maeurer, Makoto Miyara, Tarek Assi, Cristina Castilla-Llorente, Christophe Willekens, Céline Fayemi, Julien Lazarovici, Aurélien Marabelle, Lisa Derosa, Vincent Ribrag, Laurence Zitvogel
Fresh blood collected in heparinized tubes was stimulated for 22 hours at 37°C under 5% CO2 with peptide pools spanning distinctive genomic sequences of the wild-type or mutated RBD sequence (Supplementary Table 2) diluted in IFA solution (bioMérieux). The IFA solution was used as a negative control, and a mitogen (MIT) was used as a positive control. We used 15-mer peptides covering the wild-type or mutated RBD region (Supplementary Table 2). The concentration of IFNγ in the supernatant was measured using the VIDAS automated platform (VIDAS IFNγ RUO, bioMérieux). The positivity range was 0.08 to 0.3 IU/mL, and IFA positivity thresholds were defined at 0.08 IU/ml. The IFNγ response was defined as positive when the IFNγ concentration of the test was above threshold and the negative control was below threshold. All positive controls were ≥1 IU/mL.
A patent review of pharmaceutical and therapeutic applications of oxadiazole derivatives for the treatment of chronic diseases (2013–2021)
Published in Expert Opinion on Therapeutic Patents, 2022
Abbas Hassan, Abid Hussain Khan, Faiza Saleem, Haseen Ahmad, Khalid Mohammed Khan
Many growth factors like mitogens and chemotactic agents play a vital role in cell growth, migration, proliferation, and invasion. In tissue culture, the medium for growing cells generally contains serum (e.g. fetal bovine serum). The serum also stimulates the migration and invasion of cancer cells and fibroblasts. Robust activation in gene transcription occurs by the treatment of cells with serum through serum response factor (SRF). Cirrhosis, diabetic nephropathy, and heart failure are characterized by the excess deposition of cellular matrix or fibrosis. Tissue fibrosis causes systematic sclerosis and idiopathic pulmonary fibrosis. The inhibitors of Rho- and myocardin-related transcription factors and serum response factor (Rho/MRTF/SRF)-mediated gene transcription can be used for the treatment of cancer and fibrotic disease. Recently, novel 2,5-disubstituted 1,3,4-oxadiazole derivatives have been reported to inhibit Rho/MRTF/SRF-mediated gene transcription. The biological activity of the 1,3,4-oxadiazole derivatives was estimated in the SRE.L luciferase reporter assay. Compounds 21, 22, and 23 showed excellent potent activity having IC50 values 0.0012 nM, 0.019 nM, and 0.02 nM, respectively (Figure 9) [29].
What influence does mammographic density have on breast cancer occurrence?
Published in Expert Review of Anticancer Therapy, 2022
Aanchal Mathur, Sebastien Taurin
The mechanisms by which mammographic density influence the risk of developing breast cancers remain poorly understood. Multiple hypotheses have been formulated and relate to the abundance of dense tissue. One hypothesis implies that the higher number of stem cells and progenitor cells observed in dense mammary tissue is sufficient to influence the risk of breast cancer. The dysregulation of mammary stem cells or progenitor cells is one of the two main assumptions to explain the origin of breast cancers [8]. However, despite the demonstration that the dense mammary tissues harbor more stem cells and progenitor cells than less dense areas, there is no evidence of their influence on the association between mammographic density and risk of breast cancer [9]. Another hypothesis postulates that the increased mitogenic activity in dense tissue areas combined with the potential genetic damage to proliferating cells by mutagens may influence the risk of breast cancer [10]. Cell proliferation is associated with reactive oxygen species (ROS) production, promoting lipid peroxidation and genomic instability [10].