Bex3 Dimerization Regulates NGF-Dependent Neuronal Survival and Differentiation by Enhancing<i>trkA</i>Gene Transcription

Calvo, Laura; Anta, B.; López-Benito, Saray; Martín-Rodriguez, Carlos; Lee, Francis S.; Pérez, Pilar; Martı́n-Zanca, Dionisio; Arévalo, Juan Carlos

doi:10.1523/jneurosci.4646-14.2015

Cited by 32 publications

(33 citation statements)

References 52 publications

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“…Another class of NGF receptor TrkA was associated with BEX3 through the juxtamembrane domain of the receptor. Association was independent of NGF-induction, while NGF increased association in PC12 cells [65]. TrkA and BEX3 co-expressed in embryonic rat dorsal root ganglia (DRG) neurons and also form complex further suggesting a possible role BEX3 in neuron development.…”

Section: Bex Proteins In Neurotrophin Receptor Signalingmentioning

confidence: 99%

Brain-Expressed X-linked (BEX) proteins in human cancers

Kazi

Kabir

2015

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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The Brain-Expressed X-linked (BEX) family proteins are comprised of five human proteins including BEX1, BEX2, BEX3, BEX4 and BEX5. BEX family proteins are expressed in a wide range of tissues and are known to play a role in neuronal development. Recent studies suggest a role of BEX family proteins in cancers. BEX1 expression is lost in a subgroup of patients with acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). Expression of BEX1 controls cell surface receptor signaling and restores imatinib response in resistant cells. BEX2 is overexpressed in a group of breast cancer patients and also in gliomas. Increased BEX2 expression led to enhanced NF-κB signaling as well as cell proliferation. Although BEX2 acts as tumor promoter in a subset of breast cancer, BEX3 expression displayed an opposite role. Overexpression of BEX3 resulted in inhibition of tumor formation in breast cancer mouse xenograft models. The role of BEX4 and BEX5 in cancer has not yet been defined. Collectively this suggests that BEX family members have distinct roles in cancers.While BEX1 and BEX3 act as a tumor suppressors, BEX2 seems to act as an oncogene.

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Section: Bex Proteins In Neurotrophin Receptor Signalingmentioning

confidence: 99%

Brain-Expressed X-linked (BEX) proteins in human cancers

Kazi

Kabir

2015

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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“…Their interactions with p75‐related signal transduction systems help to mediate diverse biological functions (Roux & Barker, ). Depletion of rat Bex3 decreased the survival of NGF‐dependent neurons and impaired NGF‐mediated cell differentiation (Calvo et al, ). Thus, neurological impairments observed in the present patient may be caused by a BEX3 deletion.…”

Section: Discussionmentioning

confidence: 99%

An Xq22.1q22.2 nullisomy in a male patient with severe neurological impairment

Shirai

Higashi

Shimojima

et al. 2017

American J of Med Genetics Pt A

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The proteolipid protein 1 gene (PLP1) is located on chromosome Xq22.2 and is related to X-linked recessive leukoencephalopathy (Pelizaeus-Merzbacher disease: PMD). Compared to PLP1 duplications, which are a major contributor to PMD, chromosomal deletions in this region are rare and only a few PMD patients with small deletions have been reported, suggesting that large deletions of this region would cause embryonic lethality. Previously, we have reported female patients, with chromosomal deletions in this region, who showed severe developmental delays and behavioral abnormalities. In this study, we identified the first case of a male patient associated with an Xq22 nullisomy in a region proximal to PLP1. The patient showed severe neurological impairment and was bedridden. Brain magnetic resonance imaging revealed a severely reduced cerebral volume. The chromosomal region proximal to PLP1 was considered to be significantly important for brain development.

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“…The protocol used to immunize the rabbits and to purify the antibodies was carried out as previously described (Calvo et al, 2015). In brief, 3 weeks after an initial first injection of 500 μg of recombinant protein, boosts of 200 μg of recombinant protein were administered every 2 weeks.…”

Section: Generation Of Anti-arms and Anti-synembryn-b Antibodiesmentioning

confidence: 99%

ARMS/Kidins220 and synembryn-B levels regulate NGF-mediated secretion

López-Benito

Lillo

Hernández‐Hernández

et al. 2016

Journal of Cell Science

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Proper development of the nervous system requires a temporally and spatially orchestrated set of events including differentiation, synapse formation and neurotransmission. Nerve growth factor (NGF) acting through the TrkA neurotrophin receptor (also known as NTRK1) regulates many of these events. However, the molecular mechanisms responsible for NGF-regulated secretion are not completely understood. Here, we describe a new signaling pathway involving TrkA, ARMS (also known as Kidins220), synembryn-B and Rac1 in NGF-mediated secretion in PC12 cells. Whereas overexpression of ARMS blocked NGF-mediated secretion, without affecting basal secretion, a decrease in ARMS resulted in potentiation. Similar effects were observed with synembryn-B, a protein that interacts directly with ARMS. Downstream of ARMS and synembryn-B are Gαq and Trio proteins, which modulate the activity of Rac1 in response to NGF. Expression of dominant-negative Rac1 rescued the secretion defects of cells overexpressing ARMS or synembryn-B. Thus, this neurotrophin pathway represents a new mechanism responsible for NGF-regulated secretion.

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Bex3 Dimerization Regulates NGF-Dependent Neuronal Survival and Differentiation by EnhancingtrkAGene Transcription

Cited by 32 publications

References 52 publications

Brain-Expressed X-linked (BEX) proteins in human cancers

Brain-Expressed X-linked (BEX) proteins in human cancers

An Xq22.1q22.2 nullisomy in a male patient with severe neurological impairment

ARMS/Kidins220 and synembryn-B levels regulate NGF-mediated secretion

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