Neurotrophin signaling through the p75 neurotrophin receptor

Roux, Philippe P.; Barker, Philip A.

doi:10.1016/s0301-0082(02)00016-3

Cited by 643 publications

(544 citation statements)

References 398 publications

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“…Nerve growth factor (NGF) is the most studied neurotrophin, while others include brain-derived neurotrophic factor (BDNF), neurotrophin (NT)-3, and NT-4/5 [56]. The p75 neurotrophin receptor (p75NTR) and the tropomyosin-related kinase (TRK) family of receptors are known receptors of neurotrophins.…”

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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“…BDNF binding to TrkB receptor produces neurotrophic responses through rapid activation of the PI3 kinase, Ras/MAPK and PLCγ pathways, thus influence transcriptional events that has multiple effects on cell cycle, neurite outgrowth and synaptic plasticity (Qui & Green 1991, Traverse et al 1992, Cowley et al 1994, Mazzucchelli et al 2002, Rosenblum et al 2002, Chao et al 2006. Signal transduction through p75 independently gives rise to increase in JNK (c-Jun N-terminal kinase) and NF-κB (nuclear factor κB), thus triggering apoptosis (Roux & Barker 2002). Consistent with the critical role of BDNF in synaptic plasticity, BDNF is synthesized and released in an activitydependent manner (Lu 2003b).…”

Section: Molecular Mechanism Underlying Variant Bdnf Metmentioning

confidence: 99%

Impact of Genetic Variant BDNF (Val66Met) on Brain Structure and Function

Chen

Bath

McEwen

et al. 2008

Novartis Foundation Symposia

102

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A common single-nucleotide polymorphism in the human brain-derived neurotrophic factor (BDNF) gene, a methionine (Met) substitution for valine (Val) at codon 66 (Val66Met), is associated with alterations in brain anatomy and memory, but its relevance to clinical disorders is unclear. We generated a variant BDNF mouse (BDNF Met/Met ) that reproduces the phenotypic hallmarks in humans with the variant allele. Variant BDNF Met was expressed in brain at normal levels, but its secretion from neurons was defective. In this context, the BDNF Met/Met mouse represents a unique model that directly links altered activity-dependent release of BDNF to a defined set of in vivo consequences. Our subsequent analyses of these mice elucidated a phenotype that had not been established in human carriers: increased anxiety. When placed in conflict settings, BDNF Met/Met mice display increased anxiety-related behaviours that were not normalized by the antidepressant, fluoxetine. A genetic variant BDNF may thus play a key role in genetic predispositions to anxiety and depressive disorders.

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“…p75 NTR is a member of the tumour necrosis factor (TNF) receptor superfamily, and is also known as TNFRSF16 or CD271 [78]. Its structure, as determined independently by three groups, contains a cysteine-rich cytoplasmic domain, a single-pass transmembrane domain and an intracellular death domain [79][80][81].…”

Section: B Cell Malignanciesmentioning

confidence: 99%

“…It can signal in either monomeric or dimeric form upon ligand binding [82]. Unlike TrkA, p75 NTR requires the recruitment of intracellular adaptor proteins to induce signalling [78]. It has been shown to recruit a number of proteins, such actively induces pro-apoptotic signalling [88].…”

Section: B Cell Malignanciesmentioning

confidence: 99%