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L L Zhu, C H Wang, H P Yang, W H Shu
This study was carried out to investigate the expression changes of RanBP9 in tissue specimens and osteosarcoma cell strains and preliminarily explore its mechanism in osteosarcoma, so as to provide a theoretical foundation for follow-up experiments. The expression of RanBP9 in human osteosarcoma tissue specimens was detected by immunohistochemistry and the expression of RanBP9 messenger ribose nucleic acid (mRNA) in osteosarcoma cell strains was detected in real-time with polymerase chain reaction (PCR), and finally the expression of RanBP9 protein in osteosarcoma cell strains was detected by immunofluorescent staining and Western blot...
January 2016: Journal of Biological Regulators and Homeostatic Agents
Dario Palmieri, Mario Scarpa, Anna Tessari, Rexhep Uka, Foued Amari, Cindy Lee, Timothy Richmond, Claudia Foray, Tyler Sheetz, Ashley Braddom, Christin E Burd, Jeffrey D Parvin, Thomas Ludwig, Carlo M Croce, Vincenzo Coppola
Ran Binding Protein 9 (RanBP9, also known as RanBPM) is an evolutionary conserved scaffold protein present both in the nucleus and the cytoplasm of cells whose biological functions remain elusive. We show that active ATM phosphorylates RanBP9 on at least two different residues (S181 and S603). In response to IR, RanBP9 rapidly accumulates into the nucleus of lung cancer cells, but this nuclear accumulation is prevented by ATM inhibition. RanBP9 stable silencing in three different lung cancer cell lines significantly affects the DNA Damage Response (DDR), resulting in delayed activation of key components of the cellular response to IR such as ATM itself, Chk2, γH2AX, and p53...
April 5, 2016: Oncotarget
J Xie, R Gizatullin, V Vukojevic, R Leopardi
PURPOSE: Our previous study suggested that the coiled coil domain-containing 55 gene (CCDC55), also named as NSRP1 (nuclear speckle splicing regulatory protein 1 (NSRP1)), was encompassed in a haplotype block spanning over the serotonin transporter (5-HTT) gene in patients with schizophrenia (SCZ). However, the neurobiological function of CCDC55 gene remains unknown. This study aims to uncover the potential role of CCDC55 in SCZ-associated molecular pathways. EXPERIMENTAL DESIGN: Using molecular cloning, sequencing and immune blotting to identify basic properties, yeast two-hybrid screening and glutathione S-transferase (GST) pull-down assay to test protein-protein interaction, and confocal laser scanning microscopy (CSLM) to show intracellular interaction of proteins...
December 3, 2015: Neuroscience
A Rao, J Net, K Brandt, E Huang, J Freymann, E Burnside, J Kirby, E Morris, E Bonaccio, M Giger, C Jaffe, M Ganott, E Sutton, H Le-Petross, M Zuley, B Dogan, G Whitman
PURPOSE: To determine associations between radiologist-annotated MRI features and genomic measurements in breast invasive carcinoma (BRCA) from the Cancer Genome Atlas (TCGA). METHODS: 98 TCGA patients with BRCA were assessed by a panel of radiologists (TCGA Breast Phenotype Research Group) based on a variety of mass and non-mass features according to the Breast Imaging Reporting and Data System (BI-RADS). Batch corrected gene expression data was obtained from the TCGA Data Portal...
June 2015: Medical Physics
J A Woo, T Boggess, C Uhlar, X Wang, H Khan, G Cappos, A Joly-Amado, E De Narvaez, S Majid, L S Minamide, J R Bamburg, D Morgan, E Weeber, D E Kang
Molecular pathways underlying the neurotoxicity and production of amyloid β protein (Aβ) represent potentially promising therapeutic targets for Alzheimer's disease (AD). We recently found that overexpression of the scaffolding protein RanBP9 increases Aβ production in cell lines and in transgenic mice while promoting cofilin activation and mitochondrial dysfunction. Translocation of cofilin to mitochondria and induction of cofilin-actin pathology require the activation/dephosphorylation of cofilin by Slingshot homolog 1 (SSH1) and cysteine oxidation of cofilin...
2015: Cell Death & Disease
Ruizhi Wang, Hongjie Wang, Ivan Carrera, Shaohua Xu, Madepalli K Lakshmana
Brain accumulation of neurotoxic amyloid β (Aβ) peptide because of increased processing of amyloid precursor protein (APP), resulting in loss of synapses and neurodegeneration, is central to the pathogenesis of Alzheimer disease (AD). Therefore, the identification of molecules that regulate Aβ generation and those that cause synaptic damage is crucial for future therapeutic approaches for AD. We demonstrated previously that COPS5 regulates Aβ generation in neuronal cell lines in a RanBP9-dependent manner...
April 3, 2015: Journal of Biological Chemistry
Louisa M Salemi, Sandra O Loureiro, Caroline Schild-Poulter
RanBPM/RanBP9 is a ubiquitous, nucleocytoplasmic protein that is part of an evolutionary conserved E3 ubiquitin ligase complex whose function and targets in mammals are still unknown. RanBPM itself has been implicated in various cellular processes that involve both nuclear and cytoplasmic functions. However, to date, little is known about how RanBPM subcellular localization is regulated. We have conducted a systematic analysis of RanBPM regions that control its subcellular localization using RanBPM shRNA cells to examine ectopic RanBPM mutant subcellular localization without interference from the endogenously expressed protein...
2015: PloS One
Joon Seol Bae, Jason Yongha Kim, Byung-Lae Park, Hyun Sub Cheong, Jeong-Hyun Kim, Suhg Namgoong, Ji-On Kim, Chul Soo Park, Bong-Jo Kim, Cheol-Soon Lee, Migyung Lee, Woo Hyuk Choi, Tae-Min Shin, Jaeuk Hwang, Hyoung Doo Shin, Sung-Il Woo
Schizophrenia is a serious mental disorder that is affected by genetic and environmental factors. As the disease has a high heritability rate, genetic studies identifying candidate genes for schizophrenia have been conducted in various populations. The gene for human Ran‑binding protein 9 (RANBP9) is a newly discovered candidate gene for schizophrenia. As RANBP9 is a small guanosine‑5'‑triphosphate‑binding protein that interacts with the disrupted in schizophrenia 1 protein, it is considered to be an important molecule in the pathogenesis of schizophrenia...
April 2015: Molecular Medicine Reports
Jianqiang Bao, Chong Tang, Jiachen Li, Ying Zhang, Bhupal P Bhetwal, Huili Zheng, Wei Yan
As a member of the large Ran-binding protein family, Ran-binding protein 9 (RANBP9) has been suggested to play a critical role in diverse cellular functions in somatic cell lineages in vitro, and this is further supported by the neonatal lethality phenotype in Ranbp9 global knockout mice. However, the exact molecular actions of RANBP9 remain largely unknown. By inactivation of Ranbp9 specifically in testicular somatic and spermatogenic cells, we discovered that Ranbp9 was dispensable for Sertoli cell development and functions, but critical for male germ cell development and male fertility...
December 2014: PLoS Genetics
Sara C Domingues, Uwe Konietzko, Ana Gabriela Henriques, Sandra Rebelo, Margarida Fardilha, Hideo Nishitani, Roger M Nitsch, Edgar F da Cruz E Silva, Odete A B da Cruz E Silva
Proteolytic processing of the amyloid-β protein precursor (AβPP) occurs via alternative pathways, culminating with the production of the AβPP intracellular domain (AICD). AICD can translocate to the nucleus and regulate transcription, but its activity is modulated by interactions with other proteins. In the nucleus, AICD, FE65, and Tip60 associate into AFT complexes, which are targeted to nuclear spots which correspond to transcription factories. Here we report that RanBP9 interacts with the cytoplasmic domain of AβPP, through the NPXY internalization motif...
2014: Journal of Alzheimer's Disease: JAD
Ruizhi Wang, Juan Pablo Palavicini, Hongjie Wang, Panchanan Maiti, Elisabetta Bianchi, Shaohua Xu, B N Lloyd, Ken Dawson-Scully, David E Kang, Madepalli K Lakshmana
We previously demonstrated that RanBP9 overexpression increased Aβ generation and amyloid plaque burden, subsequently leading to robust reductions in the levels of several synaptic proteins as well as deficits in the learning and memory skills in a mouse model of Alzheimer's disease (AD). In the present study, we found striking reduction of spinophilin-immunoreactive puncta (52%, p<0.001) and spinophilin area (62.5%, p<0.001) in the primary cortical neurons derived from RanBP9 transgenic mice (RanBP9-Tg) compared to wild-type (WT) neurons...
September 2014: Neurobiology of Disease
Christian Barbato, Silvia Pezzola, Cinzia Caggiano, Martina Antonelli, Paola Frisone, Maria Teresa Ciotti, Francesca Ruberti
Neurodegeneration associated with amyloid β (Aβ) peptide accumulation, synaptic loss, and memory impairment are pathophysiological features of Alzheimer's disease (AD). Numerous microRNAs regulate amyloid precursor protein (APP) expression and metabolism. We previously reported that miR-101 is a negative regulator of APP expression in cultured hippocampal neurons. In this study, a search for predicted APP metabolism-associated miR-101 targets led to the identification of a conserved miR-101 binding site within the 3' untranslated region (UTR) of the mRNA encoding Ran-binding protein 9 (RanBP9)...
2014: Frontiers in Cellular Neuroscience
Manikandan Subramanian, Crystal D Hayes, Joseph J Thome, Edward Thorp, Glenn K Matsushima, Joachim Herz, Donna L Farber, Kang Liu, Madepalli Lakshmana, Ira Tabas
The phagocytosis of apoptotic cells (ACs), or efferocytosis, by DCs is critical for self-tolerance and host defense. Although many efferocytosis-associated receptors have been described in vitro, the functionality of these receptors in vivo has not been explored in depth. Using a spleen efferocytosis assay and targeted genetic deletion in mice, we identified a multiprotein complex--composed of the receptor tyrosine kinase AXL, LDL receptor-related protein-1 (LRP-1), and RAN-binding protein 9 (RANBP9)--that mediates DC efferocytosis and antigen cross-presentation...
March 2014: Journal of Clinical Investigation
H Wang, M Lewsadder, E Dorn, S Xu, M K Lakshmana
RanBP9 is a multi-domain scaffolding protein known to integrate extracellular signaling with intracellular targets. We previously demonstrated that RanBP9 enhances Aβ generation and amyloid plaque burden which results in loss of specific pre- and postsynaptic proteins in vivo in a transgenic mouse model. Additionally, we showed that the levels of spinophilin, a marker of dendritic spines were inversely proportional to the RanBP9 protein levels within the synaptosomes isolated from AD brains. In the present study, we found reduced dendritic intersections within the layer 6 pyramidal neurons of the cortex as well as the hippocampus of RanBP9 transgenic mice compared to age-matched wild-type (WT) controls at 12 months of age but not at 6months...
April 18, 2014: Neuroscience
Hongjie Wang, Ruizhi Wang, Shaohua Xu, Madepalli K Lakshmana
There is now compelling evidence that the neurodegenerative process in Alzheimer's disease (AD) begins in synapses. Loss of synaptic proteins and functional synapses in the amyloid precursor protein (APP) transgenic mouse models of AD is well established. However, what is the earliest age at which such loss of synapses occurs, and whether known markers of AD progression accelerate functional deficits is completely unknown. We previously showed that RanBP9 overexpression leads to robustly increased amyloid β peptide (Aβ) generation leading to enhanced amyloid plaque burden in a mouse model of AD...
2014: PloS One
Juan Pablo Palavicini, Hongjie Wang, Dmitriy Minond, Elisabetta Bianchi, Shaohua Xu, Madepalli K Lakshmana
Loss of synaptic proteins and functional synapses in the brains of patients with Alzheimer's disease (AD) as well as transgenic mouse models expressing amyloid-β protein precursor is now well established. However, the earliest age at which such loss of synapses occurs, and whether known markers of AD progression accelerate functional deficits is completely unknown. We previously showed that RanBP9 overexpression leads to enhanced amyloid plaque burden in a mouse model of AD. In this study, we found significant reductions in the levels of synaptophysin and spinophilin, compared with wild-type controls, in both the cortex and the hippocampus of 5- and 6-month old but not 3- or 4-month old APΔE9/RanBP9 triple transgenic mice, and not in APΔE9 double transgenic mice, nor in RanBP9 single transgenic mice...
2014: Journal of Alzheimer's Disease: JAD
Ore Francis, Fujun Han, Josephine C Adams
Ubiquitination is an essential post-translational modification that regulates signalling and protein turnover in eukaryotic cells. Specificity of ubiquitination is driven by ubiquitin E3 ligases, many of which remain poorly understood. One such is the mammalian muskelin/RanBP9/CTLH complex that includes eight proteins, five of which (RanBP9/RanBPM, TWA1, MAEA, Rmnd5 and muskelin), share striking similarities of domain architecture and have been implicated in regulation of cell organisation. In budding yeast, the homologous GID complex acts to down-regulate gluconeogenesis...
2013: PloS One
Seung-Eon Roh, Jung A Woo, Madepalli K Lakshmana, Courtney Uhlar, Vinishaa Ankala, Taylor Boggess, Tian Liu, Yun-Hwa Hong, Inhee Mook-Jung, Sang Jeong Kim, David E Kang
Mitochondrial dysfunction and synaptic damage are important features of Alzheimer's disease (AD) associated with amyloid β (Aβ) and tau. We reported previously that the scaffolding protein RanBP9, which is overall increased in brains of patients with AD and in mutant APP transgenic mice, simultaneously promotes Aβ generation and focal adhesion disruption by accelerating the endocytosis of APP and β1-integrin, respectively. Moreover, RanBP9 induces neurodegeneration in vitro and in vivo and mediates Aβ-induced neurotoxicity...
December 2013: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
Hongjie Wang, Debleena Dey, Ivan Carrera, Dmitriy Minond, Elisabetta Bianchi, Shaohua Xu, Madepalli K Lakshmana
Increased processing of amyloid precursor protein (APP) and accumulation of neurotoxic amyloid β peptide (Aβ) in the brain is central to the pathogenesis of Alzheimer's disease (AD). Therefore, the identification of molecules that regulate Aβ generation is crucial for future therapeutic approaches for AD. We demonstrated previously that RanBP9 regulates Aβ generation in a number of cell lines and primary neuronal cultures by forming tripartite protein complexes with APP, low-density lipoprotein-related protein, and BACE1, consequently leading to increased amyloid plaque burden in the brain...
September 13, 2013: Journal of Biological Chemistry
Juan Pablo Palavicini, Brandon Noel Lloyd, Crystal D Hayes, Elisabetta Bianchi, David E Kang, Ken Dawson-Scully, Madepalli K Lakshmana
RanBP9 is known to act as a scaffolding protein bringing together a variety of cell surface receptors and intracellular targets thereby regulating functions as diverse as neurite and axonal outgrowth, cell morphology, cell proliferation, myelination, gonad development, myofibrillogenesis and migration of neuronal precursors. Though RanBP9 is ubiquitously expressed in all tissues, brain is one of the organs with the highest expression levels of RanBP9. In the neurons, RanBP9 is localized mostly in the cytoplasm but also in the neurites and dendritic processes...
2013: PloS One
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