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Protein Function As Cell Surface And Nuclear Receptor In Human Diseases
Published in Debarshi Kar Mahapatra, Sanjay Kumar Bharti, Medicinal Chemistry with Pharmaceutical Product Development, 2019
Urmila Jarouliya, Raj K. Keservani
Nuclear receptors, especially thyroid hormone receptors (TRs), are also involved in pathogenesis and in the development of several types of human diseases and malignancies. It is known that mutations of TRs genes are the main cause of resistance to thyroid hormone syndrome [99]. TRs are encoded by two genes, THRA and THRB, located on chromosomes 17 and 3. Further, genetic alterations and/or aberrant expression of the TRs are reported to be associated with human malignancies such as breast, liver, thyroid, pituitary and renal cancers [100]. Some other nuclear receptor and their subfamilies are given in Table 1.2.
Salmonella
Published in Dongyou Liu, Laboratory Models for Foodborne Infections, 2017
MLST exploits the polymorphisms in selected housekeeping genes (aroC, dnaN, hemD, hisD, purE, sucA, and thrA) among Salmonella strains to determine the sequence types of the organism. MLST subtyping represents a robust technique for epidemiological and evolutionary analyses of Salmonella strains.
Nutritional Regulation of the Growth Plate
Published in Crystal D. Karakochuk, Kyly C. Whitfield, Tim J. Green, Klaus Kraemer, The Biology of the First 1,000 Days, 2017
Thyroid hormones produced by the thyroid gland, namely, 3,5,3′-triiodothyronine (T3) and thyroxine (T4), are important regulators of metabolism. T4 serves as a prohormone, which can be converted to the bioactive T3 by the enzyme type II iodothyronine deiodinase (DIO2) expressed in the thyroid and most other tissues, including the growth plate. Thyroid hormones are an important stimulator of normal linear growth. Hypothyroidism delays longitudinal bone growth and endochondral ossification, while thyrotoxicosis, which results in excessive production of thyroid hormones, accelerates both processes. Nonetheless, both hypothyroidism and thyrotoxicosis eventually lead to short stature. Thyroid hormones support bone growth by promoting the recruitment of resting chondrocyte into a proliferative zone, as well as stimulating chondrocyte hypertrophy [17]. Thyroid hormones are also essential for the normal deposition of the extracellular matrix by stimulating the production of type II and type X collagens and the synthesis of alkaline phosphatase [18]. Thyroid hormones also indirectly stimulate growth by modulating the production of GH and IGF-I. In humans with hypothyroidism and in thyroidectomized mice, both GH and IGF-I levels are decreased, and replacement of GH in hypothyroid rats or thyroid hormone receptor knockout mice partially rescues bone growth [19]. Among the four different isoforms of thyroid hormone receptors (TR-α1, -α2, -β1, -β2, encoded by two genes, THRA and THRB) found in humans, TR-α1 and -α2 are more highly expressed in the growth plate, and therefore appear to elicit much of the effect of thyroid hormone on longitudinal growth. Consistently, the homozygous deletion of THRB showed some delay in skeletal maturation, but exhibited normal growth [20], while homozygous deletion of THRA has not yet been described. So far, most cases of thyroid hormone resistance found in humans that showed postnatal growth retardation is caused by a dominant negative mutation of either TR-α or TR-β receptors [21]. Studies in humans showed that malnutrition decreases both T3 and T4 levels, and thereby slows linear growth [22]. Similarly, iodine deficiency, which is very common in some developing countries, leads to thyroid hormone deficiency and decreased linear growth. In several animal models, however, it was shown that food restriction mostly reduces T3 levels rather than T4 [23], suggesting that malnutrition may affect the conversion of T4 to T3 rather than thyroid hormone production.
Atrazine neural and reproductive toxicity
Published in Toxin Reviews, 2022
Hamidreza Sadeghnia, Sara Shahba, Alireza Ebrahimzadeh-Bideskan, Shabnam Mohammadi, Amir Mohammad Malvandi, Abbas Mohammadipour
It also alters genes associated with neuroendocrine such as CYP17A1, phosphodiesterase 10 A (PDE10A), LH, thyroid hormone receptor alpha (THRA), and adenylate cyclase 1 (ADCY1) (Weber et al. 2013, Wirbisky et al. 2015). In addition, alterations in period 1 (PER1) and period 3 (PER3) have already been reported after embryonic exposure to atrazine. PER1 and PER3 have been shown to play a role in regulating circadian rhythm (Wirbisky et al. 2016a). This herbicide has also been shown to change zebrafish's defensive and social behaviors by decreasing brain acetylcholinesterase (AChE) activity (Schmidel et al. 2014). As studies show, there is a close relationship between the cholinergic system and social stress, anxiety, depression, and resilience (Mineur et al. 2013). Thus, atrazine seems to have the potential to induce behavioral changes in humans.
Effects of bisphenol A and S on blood coagulation: in vivo, in vitro and in silico approaches in toxicodynamic
Published in Toxicology Mechanisms and Methods, 2021
Artur Paes Chagas, Beatriz Pereira Peixoto, Bianca Barros da Costa, Thamyris Almeida Moreira, Leonardo Paes Cinelli, Leandro Louback da Silva, Leandro Miranda-Alves, Clemilson Berto-Junior
Considering all harmful effects previously mentioned, BPA was prohibited by Canadian government, European commission and Food and Drug Administration (FDA) (ref.: Bisphenol S, a Bisphenol A alternative, impairs swine ovarian and adipose cell functions). For these mentioned reasons, many efforts have been made in order to gradually substitute BPA from plastic manufacture into a safe option. To achieve this, bisphenol S or BPS (Supplementary Figure 1B) was introduced in industry manufacture as a safer material, being used for the same purposes as BPA, which include baby bottles, thermal papers and food can (Oh et al. 2018). Since then, many reports have evidenced the also harmful effects of BPS: Qiu and coworkers revealed that low doses BPS led to the increase in numbers of hypothalamic GnRH3 neurons and increased expression of kiss1, gnrh3 and erα genes, being these effects abolished by estrogen receptor (ER), thyroid hormone receptors (THRs) antagonists and aromatase (AROM) blocker (Qiu et al. 2016). BPS was also show to bind to thyroid hormone receptors alpha and beta (TRα and TRβ) in silico and in vitro, with agonistic actions in the presence and absence of triiodothyronine (T3) in an in vivo model, showing it potential to interfere with thyroid hormone equilibrium (Zhang et al. 2018). Regarding the vascular system, BPS was shown to increase serum total cholesterol, triglycerides, low density lipoprotein (LDL) and very low-density lipoprotein (VLDL) in addition to reduce high density lipoprotein density (HDL) levels in rats (Pal et al. 2017).
Age-associated increase of thyroid hormone receptor β gene promoter methylation coexists with decreased gene expression
Published in Endocrine Research, 2018
Eliza Pawlik-Pachucka, Monika Budzinska, Zofia Wicik, Anna Domaszewska-Szostek, Magdalena Owczarz, Malgorzata Roszkowska-Gancarz, Magdalena Gewartowska, Monika Puzianowska-Kuznicka
Thyroid hormones co-regulate numerous processes including proliferation, differentiation, apoptosis, and cellular metabolism in developmental-, tissue type-, and pathophysiological state-dependent manner.1,2 They exert their influence by genomic and nongenomic mechanisms, utilizing protein receptors of various types, with nuclear receptors (TRs) being the most important in mediating both mechanisms.3–5 Four major TR isoforms, namely transcriptionally active TRα1, TRβ1, and TRβ2, as well as inactive TRα2, are encoded by the THRA and THRB genes. In addition, some other TR isoforms are known, including p43, the truncated form of TRα1, which regulates transcription from mitochondrial DNA.2,6