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Mechanotransduction Mechanisms of Hypertrophy and Performance with Resistance Exercise
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Andrew C. Fry, Justin X. Nicoll, Luke A. Olsen
The recruitment of mTORC1 to the lysosome may influence its activity through other mechanisms than those mentioned previously; specifically, through the lipid second messenger phosphatidic acid (PA). PA can directly activate mTORC1 through binding to its FKBP12-binding domain (184). Interestingly, phosphatidic acid increases following exercise and accumulates through the mechanosensitive properties of its upstream enzyme diacylglycerol kinase zeta (DGKζ) and phospholipase D (PLD). Indeed, the inhibition of these two enzymes attenuated mechanically driven muscle growth, while the overexpression of either PLD or DGKζ resulted in muscle hypertrophy. Moreover, PA localizes around the lysosome rendering it in close proximity to mTORC1. Outside of its ability to interact with mTORC1, PA also mediates the activity of the energy-sensing HIPPO pathway via indirect activation of yes-associated protein (YAP) through inhibition of its downstream inhibitor, long-acting thyroid stimulator (LATS) (65). Following this physical activity–induced decrease in YAP inhibition, YAP can then translocate to the nucleus, directly regulating the expression of hypertrophic genes.
Immunopathology
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
Grave’s disease, while closely related to Hashimoto’s disease (see below), may sometimes be distinguished by a greater tendency toward hyperthyroidism and proptosis in the former. Both antibody and cell-mediated autoimmune reactions have been implicated in Grave’s disease. Antibodies to thyroid microsomal antigens are present, with the important addition of antibodies binding receptors for thyroid stimulating hormone (TSH). These antibodies have been called long-acting thyroid stimulator (LATS). Binding of LATS to the TSH receptor causes increases in intracellular cyclic AMP and may induce follicular cell proliferation.
Herpes Simplex Virus and Human CNS Infections
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Marcela Kúdelová, Július Rajčáni
The family of these RNA species, referred to as LATs, map to the inverted repeats flanking the UL sequence. No replicating virus can be detected in the sensory ganglia during latent infection. In a fraction of neurons harboring latent HSV, the virus is periodically reactivated. Infectious virus is carried by anterograde axonal transport to peripheral tissues, usually to cells at or near the site of initial infection. Reactivation of virus occurs sporadically, in response to stressful stimuli such as fever, exposure to UV light, menstruation, or emotional stress. The frequency of recurrence varies in different people from monthly to less often than once per year. Depending on several factors, including the host immune status, the reactivation may be asymptomatic or lead to a recurrent lesion. Most of the data about latent infection by HSV were gained in studies on animal model systems—mice and rabbits for HSV-1 and guinea pigs for HSV-2.
Targeting Major Signaling Pathways of Bladder Cancer with Phytochemicals: A Review
Published in Nutrition and Cancer, 2021
Connor Chestnut, Dharmalingam Subramaniam, Prasad Dandawate, Subhash Padhye, John Taylor, Scott Weir, Shrikant Anant
The Hippo, or MST/WW45/LATS signaling pathway is involved in cell growth, apoptosis, and homeostasis, and has been most studied for its role in controlling organ size during embryonic development (61). This pathway is composed of a core phosphorylation cascade involving the protein kinases MST1/2, WW45, and LATS1/2, and the upstream transmembrane receptor Fat (61). The end result of this cascade is the phosphorylation and inactivation of the anti-apoptotic and pro-growth transcription factors yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) (62). Increasing evidence suggests deregulation of the Hippo pathway to be involved in BC pathogenesis. Decreased expression of MST1/2 and LATS1 has was observed in localized BC cell lines, while increased expression of YAP and TAZ was observed in high-grade and metastatic samples (61,63). It is notable that YAP1 has been implicated as a biomarker which indicates worsened prognosis and chemoresistance of BC to cisplatin (64).
Further insights into testicular germ cell tumor oncogenesis: potential therapeutic targets
Published in Expert Review of Anticancer Therapy, 2020
Paolo Chieffi, Marco De Martino, Francesco Esposito
MicroRNAs (miRNAs) are short non-coding RNA fragments that, by binding to the 3ʹUTR [61], are able to negatively regulate gene transcripts [61]. In this way, they have a critical role in several biological functions such as cellular homeostasis, development, and differentiation. Thus, recent studies have underlined that miRNA deregulation is a feature of carcinogenesis process, including TGCT instauration and progression [62–65]. To date, the histological subtypes of TGCTs have been associated with different miRNA signatures; however, few miRNAs have been observed to play key roles in TGCTs. Intriguingly, a mice strain knocked out for Dicer, the enzyme that leads to miRNA maturation, showed altered and reduced male germ cell differentiation [66]. Then, miR-372 and miR-373, which can induce the escape of p53-induced cell cycle arrest, may contribute to TGCT carcinogenesis by impairing the p53 checkpoint of cell cycle. Moreover, Voorhoeve et al. showed that these two miRNAs may induce the downregulation of LATS2, a tumor suppressor gene, representing two novel oncomiRs in TGCTs [67].
LATS2 promotes cardiomyocyte H9C2 cells apoptosis via the Prx3-Mfn2-mitophagy pathways
Published in Journal of Receptors and Signal Transduction, 2019
Yunpeng Tian, Wei Lv, Chengzhi Lu, Xiangdong Zhao, Chunguang Zhang, Haoming Song
Large tumor suppressor gene 2 (LATS2) is a key tumor suppressor gene that acts by regulating the cell cycle and DNA damage response [3,6]. In addition, LATS2 influences cellular apoptosis via the regulation of mitochondrial homeostasis, endoplasmic reticulum (ER) stress [7], calcium overload [8], and ROS-related oxidative stress [9,10]. LATS2 deficiency mediates a variety of tumor responses in cancers such as breast cancer [11], liver cancer [12], colorectal cancer [13], gastric cancer [14], lung cancer [15], and osteosarcoma [16]. Interestingly, no study is available that has established the role of LATS2 in cardiomyocyte death. Considering the causal relationship between mitochondria and cardiomyocytes [17], we ask whether LATS2 could reduce cardiomyocytes survival by regulating mitochondrial homeostasis [18].