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Regulation of the Pituitary Gland by Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
PRL and GH share a similar tertiary protein structure and utilize conserved, single-pass transmembrane receptors belonging to the type 1 cytokine receptor superfamily. The two hormones are single-chain polypeptides comprising 191–199 residues with a molecular mass of 22–23 kDa. They have two to three disulfide bridges whose location is conserved across species [44]. Both hormones, as well as their receptors, emerged by gene duplications in early vertebrate evolution. The two hormones are involved in multiple physiologic processes, including development, growth, reproduction, and metabolism, with few overlapping functions. Despite their many similarities, GH and PRL are produced by distinct anterior pituitary cells, and differ in the controls of their expression, synthesis, release, and actions.
Soluble Mediators of Cellular Cooperation: The Cytokines
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
Almost all of the cytokines described above have at least been suggested by in vitro data to play a role in some aspect of hemopoiesis or lymphopoiesis. However, the type I cytokine receptor family, or the hemopoietic growth factor receptor family, is comprised of IL-2R (β and yc), IL-3R, −5R, −6R and GM-CSFR (both a and β chains), and IL-4R, −7R, EPOR, G-CSFR, LIFR, and ciliary neurotrophic factor (see below). This family is defined by two structural elements: at the amino terminus they have a sequence containing conserved cysteines and tryptophan in certain positions; at the carboxyl terminus they have a Trp-Ser-X-Ser-Trp. This family also includes receptors for growth hormone and prolactin which are structurally similar except that they lack the carboxyl terminal motif. These receptors act via a tyrosine kinase pathway but do not have intrinsic tyrosine kinase activity. Presumably, before or after ligand binding, they associate with other molecules which then further transduce a signal or are themselves tyrosine kinases.
Physiology of the Pituitary Gland
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Mária Hérincs, Karen Young, Márta Korbonits
GH acts via the GH receptor (GHR), which belongs to the type I cytokine receptor family. GH binding to the dimerized GHR activates Janus kinase 2 (JAK2) and signal transducer and activator of transcription (STAT) (Figure 56.2). While GH exerts its direct metabolic effects via this pathway, other effects are exerted through insulin-like growth factor type 1 (IGF-1), synthesized not only in the liver but in all local tissues, and responsible for the growth effects of the hormone. IGF-1 binds to the type 1 IGF receptor, which belongs to the membrane-bound tyrosine kinase receptor family.8
JAK inhibitors in dermatology: the road travelled and path ahead, a narrative review
Published in Expert Review of Clinical Pharmacology, 2023
Aishwarya Muddebihal, Ananta Khurana, Kabir Sardana
Janus kinases (JAK) are nonreceptor intracellular tyrosine kinases that modify cytokine mediated signaling through JAK- signal transducers and activator of transcription (STAT) [1]. The JAK-STAT pathway has important role in innate and adaptive immune responses, as well as certain physiological functions. Its role as a signaling pathway was first discovered for IFN-γ [2]. It is now known that the JAK family of kinases is crucial for signaling via type I/II cytokine receptors. Prominent ligands of type I cytokine receptor are: cytokines (IL-2, IL-6, IL-12, IL-13, IL-23, IL-1β, IL-1α, TNF-α, TNF-β etc), erythropoietin, thrombopoietin, granulocyte-colony–stimulating factor, growth hormone, prolactin and leptin, while important type II cytokines are IL-10 family and type I, II and III interferons. Numerous cutaneous inflammatory dermatoses mediated by these cytokines depend on JAK STAT signaling pathway and thus are potentially amenable to treatment with JAK inhibitors (JAKinibs).
Therapeutic targeting of the IL-13 pathway in skin inflammation
Published in Expert Review of Clinical Immunology, 2021
IL-4 and IL-13 share a common receptor subunit, the IL-4Rα chain [16,76]. IL-4 signals by binding two different types of receptors [16,76]. On one side, type I IL-4 receptor consists of the IL-4Rα subunit and the common gamma chain (γc), a member of the type I cytokine receptor common to receptor complexes of the IL-2 family cytokines that is expressed on most lymphocyte populations; after binding, conformational changes in IL-4Rα and γc tails lead to the phosphorylation of the associated Jak kinases JAK1 and JAK3, respectively [16,76–79]. On the other side, there is the type II IL-4 receptor or IL-13 receptor, which is shared by both IL-4 and IL-13; it consists on an IL-4Rα chain plus an IL-13Rα1 chain [16,76]. The binding affinity of IL-4 for IL-4Rα is much higher than IL-13 for the IL-13Rα1; thus, IL-4 would out-compete IL-13 for type II IL-4 receptor availability if both were present at similar tissue concentrations [76]. The γc receptor type I subunit is predominantly expressed in hematopoietic cells whereas expression of IL-13Rα1 chain from type II receptor is higher in structural tissue cells such as KCs [16,80].
Cytokine control of megakaryopoiesis
Published in Growth Factors, 2018
Kira Behrens, Warren S. Alexander
The MPNs are three distinct disorders, essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF), that are characterized by activated cytokine receptor signalling pathways caused by three major classes of mutation. Activating mutations in JAK2, a key mediator of Tpo signalling, as well as that of Epo and other cytokines, are the most prevalent, particularly the JAK2 V617F mutation, and account for around two-thirds of MPN, including almost all PV. Several in vitro and in vivo studies have demonstrated that expression of a type-I cytokine receptor, such as Mpl or the Epo receptor, is crucial for the development of JAK2 mutant-induced disease (Lu et al., 2005; Sangkhae et al., 2014). Mutations in the calreticulin (CALR) gene are also common in ET and PMF. These mutations induce a frameshift to a specific alternative reading frame, resulting in a new C-terminal sequence with a positively charged tail that binds exclusively to, and constitutively activates, the Mpl receptor, explaining the megakaryocytic phenotype of the diseases (Araki et al., 2016; Chachoua et al., 2016; Klampfl et al., 2013). Activating mutations in MPL itself are also observed in MPN, most frequently substitution of the W515 residue in the transmembrane domain, a key residue in regulating dimerization, although rare mutations in the extracellular or cytoplasmic regions can also be found (Defour et al., 2013; Milosevic Feenstra et al., 2016; Pikman et al., 2006).