Blurring Boundaries: Receptor Tyrosine Kinases as functional G Protein-Coupled Receptors

Crudden, Caitrin; Shibano, Takashi; Song, Dawei; Suleymanova, Naida; Girnita, Leonard

doi:10.1016/bs.ircmb.2018.02.006

Cited by 34 publications

(31 citation statements)

References 225 publications

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“…Prominent RTK downstream signalling components and pathways include ERK1/2, p38 and JNK in the family of mitogen-activated protein (MAP) kinases, PI3K-AKT-mTOR and PLCγ as well as a branch of STAT signalling 220 . In addition, RTKs extensively cross-talk with other receptor systems and may signal through G proteins, GRKs, and β-arrestins to control various cellular responses 221 . Designated subtypes of class II and class III RTKs, including platelet-derived growth factor alpha receptor (PDFGRα), the insulin receptor (IR) and insulin-like growth factor receptor (IGFIR) operate in primary cilia to control specific processes in cells and tissues 222, 223 (Figure 5).…”

Section: Ciliary Rtk Signallingmentioning

confidence: 99%

Cellular signalling by primary cilia in development, organ function and disease

et al. 2019

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Primary cilia project in a single copy from the surface of most vertebrate cell types; they detect and transmit extracellular cues to regulate diverse cellular processes during development and to maintain tissue homeostasis. The sensory capacity of primary cilia relies on the coordinated trafficking and temporal localization of specific receptors and associated signal transduction modules in the cilium. The canonical hedgehog (HH) pathway, for example, is a bona fide ciliary signalling system that regulates cell fate and self-renewal in development and tissue homeostasis. Specific receptors and associated signal transduction proteins can also localize to primary cilia in a cell type-dependent manner; available evidence suggests that the ciliary constellation of these proteins can temporally change to allow the cell to adapt to specific developmental and homeostatic cues. Consistent with important roles for primary cilia in signalling, mutations that lead to their dysfunction underlie a pleiotropic group of diseases and syndromic disorders termed ciliopathies, which affect many different tissues and organs of the body. In this review we highlight central mechanisms by which primary cilia coordinate HH, G-protein-coupled receptor, WNT, receptor tyrosine kinase and TGFβ/BMP signalling, and illustrate how defects in the balanced output of ciliary signalling events are coupled to developmental disorders and disease progression. Opening section The primary cilium is a microtubule-based, non-motile organelle that extends as a solitary unit from the basal body (derived from the centrosomal mother centriole of most cell types

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Section: Ciliary Rtk Signallingmentioning

confidence: 99%

Cellular signalling by primary cilia in development, organ function and disease

et al. 2019

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“…Subsequently, the activated RTK complex phosphorylates downstream targets that include different intracellular kinases (the MAP kinase family, PI3K-AKT pathway kinases, PL Cγ , and others), which exert the effects induced by specific ligand molecules (Crudden et al, 2018). Signaling through PDGFRα, insulin receptor (IR), and IGF-1 receptor (IGF-1R) is tightly connected to PC (Christensen et al, 2012) (Figure 3D).…”

Section: Receptor Tyrosine Kinasesmentioning

confidence: 99%

Primary Ciliary Signaling in the Skin—Contribution to Wound Healing and Scarring

Hosio

Jaks

Lagus

et al. 2020

Front. Cell Dev. Biol.

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“…Some components of these kinase-activated pathways (e.g., mTOR complex 1, ERK1/2, and JNK) also trigger feedback control loops, by desensitizing the kinase signaling cascades [27]. The IGF-1R, as many other RTKs, is able to initiate downstream signaling completely independently of ligand-binding through means of transactivation by other plasma-membrane receptors such as other RTKs, G-protein-coupled receptors (GPCRs), or integrins [30,31]. Likewise, the IGF-1R could activate downstream non-kinase signaling pathways in a kinase-independent manner by employing the signal transduction machinery traditionally known to be used by the GPCR (e.g., the GRK/β-arrestin system and G-proteins) [32,33].…”

Section: Role Of Igf-1r Signaling In the Pathogenesis Of Dm And Cancermentioning

confidence: 99%

Non-Coding RNAs in IGF-1R Signaling Regulation: The Underlying Pathophysiological Link between Diabetes and Cancer

Chen

Chi

et al. 2019

Cells

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The intricate molecular network shared between diabetes mellitus (DM) and cancer has been broadly understood. DM has been associated with several hormone-dependent malignancies, including breast, pancreatic, and colorectal cancer (CRC). Insulin resistance, hyperglycemia, and inflammation are the main pathophysiological mechanisms linking DM to cancer. Non-coding RNAs (ncRNAs), particularly microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), are widely appreciated as pervasive regulators of gene expression, governing the evolution of metabolic disorders, including DM and cancer. The ways ncRNAs affect the development of DM complicated with cancer have only started to be revealed in recent years. Insulin-like growth factor 1 receptor (IGF-1R) signaling is a master regulator of pathophysiological processes directing DM and cancer. In this review, we briefly summarize a number of well-known miRNAs and lncRNAs that regulate the IGF-1R in DM and cancer, respectively, and further discuss the potential underlying molecular pathogenesis of this disease association.

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Blurring Boundaries: Receptor Tyrosine Kinases as functional G Protein-Coupled Receptors

Cited by 34 publications

References 225 publications

Cellular signalling by primary cilia in development, organ function and disease

Cellular signalling by primary cilia in development, organ function and disease

Primary Ciliary Signaling in the Skin—Contribution to Wound Healing and Scarring

Non-Coding RNAs in IGF-1R Signaling Regulation: The Underlying Pathophysiological Link between Diabetes and Cancer

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