Nedd4 Family Interacting Protein 1 (Ndfip1) Is Required for Ubiquitination and Nuclear Trafficking of BRCA1-associated ATM Activator 1 (BRAT1) during the DNA Damage Response

Low, Ley-Hian; Chow, Yuh-Lit; Li, Yijia; Goh, Choo-Peng; Putz, Ulrich; Silke, John; Ouchi, Toru; Howitt, Jason; Tan, Seong‐Seng

doi:10.1074/jbc.m114.613687

Cited by 27 publications

(18 citation statements)

References 25 publications

(50 reference statements)

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“…For example, MRE11 and NBS1, components of MRE11-Rad50-NBS1 complex for DNA damage sensing and activation of ATM kinase, were identified as candidates associated with TCTP. In addition to DNA damage response signaling, proteins involved in double-strand break repair such as BRCA1-interacting protein BRAT1 44 , 45 and BRCA2-associated protein BCCIP 46 showed up in our TCTP interactome, hinting the potential role of TCTP in the maintenance of genome stability in HeLa cells. In fact, TCTP has been implicated in both NHEJ and HR repair.…”

Section: Discussionmentioning

confidence: 89%

Identification of translationally controlled tumor protein in promotion of DNA homologous recombination repair in cancer cells by affinity proteomics

Hui

Zhang

et al. 2017

Oncogene

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Translationally controlled tumor protein(TCTP) has been implicated in the regulation of apoptosis, DNA repair and drug resistance. However, the underlying molecular mechanisms are poorly defined. To better understand the molecular mechanisms underlying TCTP involved in cellular processes, we performed an affinity purification-based proteomic profiling to identify proteins interacting with TCTP in human cervical cancer HeLa cells. We found that a group of proteins involved in DNA repair are enriched in the potential TCTP interactome. Silencing TCTP by short hairpin RNA in breast carcinoma MCF-7 cells leads to the declined repair efficiency for DNA double-strand breaks on the GFP-Pem1 reporter gene by homologous recombination, the persistent activation and the prolonged retention of γH2AX and Rad51 foci following ionizing radiation. Reciprocal immunoprecipitations indicated that TCTP forms complexes with Rad51 in vivo, and the stability maintenance of Rad51 requires TCTP in MCF-7 cells under normal cell culture conditions. Moreover, inactivation of TCTP by sertraline treatment enhances UVC irradiation-induced apoptosis in MCF-7 cells, and causes sensitization to DNA-damaging drug etoposide and DNA repair inhibitor olaparib. Thus, we have identified an important role of TCTP in promoting DNA double-stand break repair via facilitating DNA homologous recombination processes and highlighted the great potential of TCTP as a drug target to enhance conventional chemotherapy for cancer patients with high levels of TCTP expression.

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Section: Discussionmentioning

confidence: 89%

Identification of translationally controlled tumor protein in promotion of DNA homologous recombination repair in cancer cells by affinity proteomics

Hui

Zhang

et al. 2017

Oncogene

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“…Nedd4 family interacting protein 1 (Ndfip1), also known as Nedd4 WW-domain-binding protein 5 (N4WBP5), plays a role in neuroprotection, through mediating ubiquitination of target proteins in neuronal injury (Howitt et al, 2009 ; Goh et al, 2014 ; Low et al, 2015 ). Interestingly, DMT1 is one of the Ndfip1 target proteins, and Ndfip1 can degrade DMT1 protein through ubiquitination pathway (Foot et al, 2008 ; Howitt et al, 2009 ; Garrick et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

Lower Expression of Ndfip1 Is Associated With Alzheimer Disease Pathogenesis Through Decreasing DMT1 Degradation and Increasing Iron Influx

Tian

Zheng

et al. 2018

Front. Aging Neurosci.

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We have previously reported that high expression of divalent metal transporter 1 (DMT1) plays a crucial role in iron dyshomeostasis and β-amyloid (Aβ) peptide generation in the brain of Alzheimer’s disease (AD). Recent studies have shown that Nedd4 family interacting protein 1 (Ndfip1) can degrade DMT1 through ubiquitination pathway and reduce the accumulation of intracellular iron. The present study aims to evaluate whether Ndfip1 is involved in AD pathogenesis through mediating DMT1 degradation and iron metabolism. β-amyloid precursor protein/presenilin 1 (APP/PS1) transgenic mouse and Ndfip1 transfected SH-SY5Y cells were used in this study. Immunohistochemistry and Western blot were performed to examine the distribution and expression levels of Ndfip1 and DMT1. In addition, ELISA and calcein fluorescence were carried out for analyzing the levels of Aβ peptide and iron influx, respectively. The results showed that Ndfip1 immunoreactivity was decreased in the cortex and hippocampus of APP/PS1 mice, compared with wild type (WT) controls. Colocalization of Ndfip1 and Aβ within senile plaques could be observed. Immunoblot analyses showed that low expression of Ndfip1 and high expression of DMT1 proteins were detected in APP/PS1 mouse brain, compared with age-matched WT animals. Overexpression of Ndfip1 down-regulated DMT1 expression, and reduced iron influx and Aβ secretion in SH-SY5Y cells. Further, overexpressed Ndfip1 significantly attenuated iron-induced cell damage in Ndfip1 transfected cells. The present study suggests that lower expression of Ndfip1 might be associated with the pathogenesis of AD, through decreasing DMT1 degradation and increasing iron accumulation in the brain.

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“…Similarly, NDFIP1 (NEDD4 Family Interacting Protein 1, Figure 5H) modulates EGFR signaling through multiple pathways. NDFIP1 may regulate the ratio of AKT1-to-MAPK8 signaling in response to EGF [45] . AKT signaling is associated with nAChR, however no direct association between nicotine and NDFIP1 has been described.…”

Section: Resultsmentioning

confidence: 99%

Isobaric Tag‐Based Protein Profiling of a Nicotine‐Treated Alpha7 Nicotinic Receptor‐Null Human Haploid Cell Line

Paulo

Gygi

2018

Proteomics

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Nicotinic acetylcholine receptors (nAChR), the primary cell surface targets of nicotine, have implications in various neurological disorders. Here we investigate the proteome-wide effects of nicotine on human haploid cell lines (wildtype HAP1 and α7KO-HAP1) to address differences in nicotine-induced protein abundance profiles between these cell lines. We performed an SPS-MS3-based TMT10-plex experiment arranged in a 2-3-2-3 design with two replicates for the untreated samples and three for the treated samples for each cell line. We quantified 8,775 proteins across all 10 samples, of which several hundred differed significantly in abundance. Comparing α7KO-HAP1 and HAP1wt cell lines revealed significant protein abundance alterations, however we also measured differences resulting from nicotine treatment in both cell lines. Among proteins with increased abundance levels due to nicotine treatment included those previously identified: APP, APLP2, and ITM2B. The magnitude of these changes was greater in HAP1wt compared to the α7KO-HAP1 cell line, implying a potential role of the α7 nAChR in HAP1 cells. Moreover, the data revealed that membrane proteins and proteins commonly associated with neurons were predominant among those with altered abundance. This study, which is the first TMT-based proteome profiling of HAP1 cells, defines further the effects of nicotine on non-neuronal cellular proteomes.

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Nedd4 Family Interacting Protein 1 (Ndfip1) Is Required for Ubiquitination and Nuclear Trafficking of BRCA1-associated ATM Activator 1 (BRAT1) during the DNA Damage Response

Cited by 27 publications

References 25 publications

Identification of translationally controlled tumor protein in promotion of DNA homologous recombination repair in cancer cells by affinity proteomics

Identification of translationally controlled tumor protein in promotion of DNA homologous recombination repair in cancer cells by affinity proteomics

Lower Expression of Ndfip1 Is Associated With Alzheimer Disease Pathogenesis Through Decreasing DMT1 Degradation and Increasing Iron Influx

Isobaric Tag‐Based Protein Profiling of a Nicotine‐Treated Alpha7 Nicotinic Receptor‐Null Human Haploid Cell Line

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