RanBPM interacts with TβRI, TRAF6 and curbs TGF induced nuclear accumulation of TβRI

Zhang, Junwen; Ma, Wei; Tian, Shuo; Fan, Zhenzhen; Yang, Xia; Zhao, Qinghao; Tan, Kuan Onn; Chen, Hong; Deng, Chao; Huang, Baojia

doi:10.1016/j.cellsig.2013.09.019

Cited by 15 publications

(14 citation statements)

References 50 publications

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“…Several studies have suggested that RanBPM functions to prevent cell transformation through restricting the activation of several signalling pathways that promote tumourigenesis [5,29,38,41,50–52,81,86,95]. Work in our laboratory has suggested a tumour suppressor role for RanBPM through an inhibition of ERK signalling.…”

Section: Ranbpm In Cancermentioning

confidence: 98%

Cell signalling pathway regulation by RanBPM: molecular insights and disease implications

Salemi¹,

Maitland²,

McTavish³

et al. 2017

Open Biol.

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RanBPM (Ran-binding protein M, also called RanBP9) is an evolutionarily conserved, ubiquitous protein which localizes to both nucleus and cytoplasm. RanBPM has been implicated in the regulation of a number of signalling pathways to regulate several cellular processes such as apoptosis, cell adhesion, migration as well as transcription, and plays a critical role during development. In addition, RanBPM has been shown to regulate pathways implicated in cancer and Alzheimer's disease, implying that RanBPM has important functions in both normal and pathological development. While its functions in these processes are still poorly understood, RanBPM has been identified as a component of a large complex, termed the CTLH (C-terminal to LisH) complex. The yeast homologue of this complex functions as an E3 ubiquitin ligase that targets enzymes of the gluconeogenesis pathway. While the CTLH complex E3 ubiquitin ligase activity and substrates still remain to be characterized, the high level of conservation between the complexes in yeast and mammals infers that the CTLH complex could also serve to promote the degradation of specific substrates through ubiquitination, therefore suggesting the possibility that RanBPM's various functions may be mediated through the activity of the CTLH complex.

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Section: Ranbpm In Cancermentioning

confidence: 98%

Cell signalling pathway regulation by RanBPM: molecular insights and disease implications

Salemi¹,

Maitland²,

McTavish³

et al. 2017

Open Biol.

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“…Like the TACE-cleaved TβRI intracellular fragment, the presenilin 1–released fragment stimulates the expression of cell-invasion-related genes, such as Snai1 (encoding Snail) and Jag1 (Jagged1) (Gudey et al 2014). A recent study reported that TRAF6-mediated TβRI cleavage is regulated by the scaffold protein Ran-binding protein M (RanBPM), which interacts with TβRI and prevents its association with TRAF6 and its subsequent cleavage and nuclear accumulation of the intracellular fragment (Zhang et al 2014). As this fragment was observed in the nuclei of malignant tumors (Mu et al 2011; Gudey et al 2014), these results underscore the role of the finely regulated proteolytic cleavage of TβRI in tumorigenesis.…”

Section: Receptors: Activation and Regulation Of Their Activitiesmentioning

confidence: 99%

TGF-β Signaling from Receptors to Smads

Hata

Chen

2016

Cold Spring Harb Perspect Biol

686

527

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Transforming growth factor β (TGF-β) and related growth factors are secreted pleiotropic factors that play critical roles in embryogenesis and adult tissue homeostasis by regulating cell proliferation, differentiation, death, and migration. The TGF-β family members signal via heteromeric complexes of type I and type II receptors, which activate members of the Smad family of signal transducers. The main attribute of the TGF-β signaling pathway is context-dependence. Depending on the concentration and type of ligand, target tissue, and developmental stage, TGF-β family members transmit distinct signals. Deregulation of TGF-β signaling contributes to developmental defects and human diseases. More than a decade of studies have revealed the framework by which TGF-βs encode a context-dependent signal, which includes various positive and negative modifiers of the principal elements of the signaling pathway, the receptors, and the Smad proteins. In this review, we first introduce some basic components of the TGF-β signaling pathways and their actions, and then discuss posttranslational modifications and modulatory partners that modify the outcome of the signaling and contribute to its context-dependence, including small noncoding RNAs.

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“…Functional classification of the deregulated genes revealed that a significant subset of candidate genes is involved in cellular and metabolic signaling (Figures S6A–S6C). Although we could not link these candidates to known Ret signaling components, some of the affected genes, including vis (Wang and Mann, 2003), RanBPM (Zhang et al, 2014), and CG8768 (Kim and Marqués, 2010), have previously been implicated in TGF-β signaling.…”

Section: Resultsmentioning

confidence: 95%

Ret and Substrate-Derived TGF-β Maverick Regulate Space-Filling Dendrite Growth in Drosophila Sensory Neurons

Hoyer

Zielke

et al. 2018

Cell Reports

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Summary Dendrite morphogenesis is a highly regulated process that gives rise to stereotyped receptive fields, which are required for proper neuronal connectivity and function. Specific classes of neurons, including Drosophila class IV dendritic arborization (C4da) neurons, also feature complete space-filling growth of dendrites. In this system, we have identified the substrate-derived TGF-β ligand maverick (mav) as a developmental signal promoting space-filling growth through the neuronal Ret receptor. Both are necessary for radial spreading of C4da neuron dendrites, and Ret is required for neuronal uptake of Mav. Moreover, local changes in Mav levels result in directed dendritic growth toward regions with higher ligand availability. Our results suggest that Mav acts as a substrate-derived secreted signal promoting dendrite growth within not-yet-covered areas of the receptive field to ensure space-filling dendritic growth.

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RanBPM interacts with TβRI, TRAF6 and curbs TGF induced nuclear accumulation of TβRI

Cited by 15 publications

References 50 publications

Cell signalling pathway regulation by RanBPM: molecular insights and disease implications

Cell signalling pathway regulation by RanBPM: molecular insights and disease implications

TGF-β Signaling from Receptors to Smads

Ret and Substrate-Derived TGF-β Maverick Regulate Space-Filling Dendrite Growth in Drosophila Sensory Neurons

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