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  1. Book ; Online: Vertical Federated Learning over Cloud-RAN

    Shi, Yuanming / Xia, Shuhao / Zhou, Yong / Mao, Yijie / Jiang, Chunxiao / Tao, Meixia

    Convergence Analysis and System Optimization

    2023  

    Abstract: ... Cloud-RAN) based vertical FL system to enable fast and accurate model aggregation by leveraging over ...

    Abstract Vertical federated learning (FL) is a collaborative machine learning framework that enables devices to learn a global model from the feature-partition datasets without sharing local raw data. However, as the number of the local intermediate outputs is proportional to the training samples, it is critical to develop communication-efficient techniques for wireless vertical FL to support high-dimensional model aggregation with full device participation. In this paper, we propose a novel cloud radio access network (Cloud-RAN) based vertical FL system to enable fast and accurate model aggregation by leveraging over-the-air computation (AirComp) and alleviating communication straggler issue with cooperative model aggregation among geographically distributed edge servers. However, the model aggregation error caused by AirComp and quantization errors caused by the limited fronthaul capacity degrade the learning performance for vertical FL. To address these issues, we characterize the convergence behavior of the vertical FL algorithm considering both uplink and downlink transmissions. To improve the learning performance, we establish a system optimization framework by joint transceiver and fronthaul quantization design, for which successive convex approximation and alternate convex search based system optimization algorithms are developed. We conduct extensive simulations to demonstrate the effectiveness of the proposed system architecture and optimization framework for vertical FL.

    Comment: 32 pages, 7 figures
    Keywords Computer Science - Information Theory ; Computer Science - Machine Learning ; Electrical Engineering and Systems Science - Signal Processing
    Subject code 006
    Publishing date 2023-05-04
    Publishing country us
    Document type Book ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: RAN Translation in Huntington Disease.

    Bañez-Coronel, Monica / Ayhan, Fatma / Tarabochia, Alex D / Zu, Tao / Perez, Barbara A / Tusi, Solaleh Khoramian / Pletnikova, Olga / Borchelt, David R / Ross, Christopher A / Margolis, Russell L / Yachnis, Anthony T / Troncoso, Juan C / Ranum, Laura P W

    Neuron

    2015  Volume 88, Issue 4, Page(s) 667–677

    Abstract: ... These sense and antisense repeat-associated non-ATG (RAN) translation proteins accumulate most abundantly ... matter, and, in juvenile-onset cases, also the cerebellum. RAN protein accumulation and aggregation are ... length dependent, and individual RAN proteins are toxic to neural cells independent of RNA effects ...

    Abstract Huntington disease (HD) is caused by a CAG ⋅ CTG expansion in the huntingtin (HTT) gene. While most research has focused on the HTT polyGln-expansion protein, we demonstrate that four additional, novel, homopolymeric expansion proteins (polyAla, polySer, polyLeu, and polyCys) accumulate in HD human brains. These sense and antisense repeat-associated non-ATG (RAN) translation proteins accumulate most abundantly in brain regions with neuronal loss, microglial activation and apoptosis, including caudate/putamen, white matter, and, in juvenile-onset cases, also the cerebellum. RAN protein accumulation and aggregation are length dependent, and individual RAN proteins are toxic to neural cells independent of RNA effects. These data suggest RAN proteins contribute to HD and that therapeutic strategies targeting both sense and antisense genes may be required for efficacy in HD patients. This is the first demonstration that RAN proteins are expressed across an expansion located in an open reading frame and suggests RAN translation may also contribute to other polyglutamine diseases.
    MeSH term(s) Adult ; Aged, 80 and over ; Brain/metabolism ; Case-Control Studies ; Cerebellum/metabolism ; Child ; Female ; Frontal Lobe/metabolism ; HEK293 Cells ; Humans ; Huntingtin Protein ; Huntington Disease/genetics ; Huntington Disease/metabolism ; Male ; Middle Aged ; Neostriatum/metabolism ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Peptides/metabolism ; Protein Aggregation, Pathological/metabolism ; Protein Biosynthesis ; RNA, Antisense/genetics ; RNA, Antisense/metabolism ; Trinucleotide Repeat Expansion/genetics ; Young Adult
    Chemical Substances HTT protein, human ; Huntingtin Protein ; Nerve Tissue Proteins ; Peptides ; RNA, Antisense ; polyalanine (25191-17-7) ; polyleucine (25248-98-0) ; polyserine (25821-52-7) ; polyglutamine (26700-71-0) ; polycysteine (62488-11-3)
    Language English
    Publishing date 2015-11-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2015.10.038
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Metformin inhibits RAN translation through PKR pathway and mitigates disease in

    Zu, Tao / Guo, Shu / Bardhi, Olgert / Ryskamp, Daniel A / Li, Jian / Khoramian Tusi, Solaleh / Engelbrecht, Avery / Klippel, Kelena / Chakrabarty, Paramita / Nguyen, Lien / Golde, Todd E / Sonenberg, Nahum / Ranum, Laura P W

    Proceedings of the National Academy of Sciences of the United States of America

    2020  Volume 117, Issue 31, Page(s) 18591–18599

    Abstract: Repeat associated non-AUG (RAN) translation is found in a growing number of microsatellite ... expansion diseases, but the mechanisms remain unclear. We show that RAN translation is highly regulated ...

    Abstract Repeat associated non-AUG (RAN) translation is found in a growing number of microsatellite expansion diseases, but the mechanisms remain unclear. We show that RAN translation is highly regulated by the double-stranded RNA-dependent protein kinase (PKR). In cells, structured CAG, CCUG, CAGG, and G
    MeSH term(s) Amyotrophic Lateral Sclerosis/metabolism ; Animals ; Brain/metabolism ; Brain/pathology ; C9orf72 Protein/genetics ; C9orf72 Protein/metabolism ; Disease Models, Animal ; Frontotemporal Dementia/metabolism ; Humans ; Metformin/pharmacology ; Mice ; Mice, Transgenic ; Microsatellite Repeats/genetics ; Protein Biosynthesis/drug effects ; eIF-2 Kinase/genetics ; eIF-2 Kinase/metabolism
    Chemical Substances C9orf72 Protein ; Metformin (9100L32L2N) ; eIF-2 Kinase (EC 2.7.11.1)
    Language English
    Publishing date 2020-07-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2005748117
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The alternative initiation factor eIF2A plays key role in RAN translation of myotonic dystrophy type 2 CCUG•CAGG repeats.

    Tusi, Solaleh Khoramian / Nguyen, Lien / Thangaraju, Kiruphagaran / Li, Jian / Cleary, John D / Zu, Tao / Ranum, Laura P W

    Human molecular genetics

    2021  Volume 30, Issue 11, Page(s) 1020–1029

    Abstract: Repeat-associated non-ATG (RAN) proteins have been reported in 11 microsatellite expansion ... disorders but the factors that allow RAN translation to occur and the effects of different repeat motifs and ... alternative AUG-like initiation codons are unclear. We studied the mechanisms of RAN translation across ...

    Abstract Repeat-associated non-ATG (RAN) proteins have been reported in 11 microsatellite expansion disorders but the factors that allow RAN translation to occur and the effects of different repeat motifs and alternative AUG-like initiation codons are unclear. We studied the mechanisms of RAN translation across myotonic dystrophy type 2 (DM2) expansion transcripts with (CCUG) or without (CAGG) efficient alternative AUG-like codons. To better understand how DM2 LPAC and QAGR RAN proteins are expressed, we generated a series of CRISPR/Cas9-edited HEK293T cell lines. We show that LPAC and QAGR RAN protein levels are reduced in protein kinase R (PKR)-/- and PKR-like endoplasmic reticulum kinase (PERK)-/- cells, with more substantial reductions of CAGG-encoded QAGR in PKR-/- cells. Experiments using mutant eIF2α-S51A HEK293T cells show that p-eIF2α is required for QAGR production. In contrast, LPAC levels were only partially reduced in these cells, suggesting that both non-AUG and close-cognate initiation occur across CCUG RNAs. Overexpression of the alternative initiation factor eIF2A increases LPAC and QAGR protein levels but, notably, has a much larger effect on QAGR expressed from CAGG-expansion RNAs that lack efficient close-cognate codons. The effects of eIF2A on increasing LPAC are consistent with previous reports that eIF2A affects CUG-initiation translation. The observation that eIF2A also increases QAGR proteins is novel because CAGG expansion transcripts do not contain CUG or similarly efficient close-cognate AUG-like codons. For QAGR but not LPAC, the eIF2A-dependent increases are not seen when p-eIF2α is blocked. These data highlight the differential regulation of DM2 RAN proteins and eIF2A as a potential therapeutic target for DM2 and other RAN diseases.
    MeSH term(s) CRISPR-Cas Systems/genetics ; DNA Repeat Expansion/genetics ; Eukaryotic Initiation Factor-2/genetics ; HEK293 Cells ; Humans ; Microsatellite Repeats/genetics ; Myotonic Dystrophy/genetics ; Myotonic Dystrophy/physiopathology ; Protein Biosynthesis/genetics ; eIF-2 Kinase/genetics
    Chemical Substances Eukaryotic Initiation Factor-2 ; EIF2AK2 protein, human (EC 2.7.11.1) ; EIF2AK3 protein, human (EC 2.7.11.1) ; eIF-2 Kinase (EC 2.7.11.1)
    Language English
    Publishing date 2021-04-15
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1108742-0
    ISSN 1460-2083 ; 0964-6906
    ISSN (online) 1460-2083
    ISSN 0964-6906
    DOI 10.1093/hmg/ddab098
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: CCG•CGG interruptions in high-penetrance SCA8 families increase RAN translation and protein toxicity.

    Perez, Barbara A / Shorrock, Hannah K / Banez-Coronel, Monica / Zu, Tao / Romano, Lisa El / Laboissonniere, Lauren A / Reid, Tammy / Ikeda, Yoshio / Reddy, Kaalak / Gomez, Christopher M / Bird, Thomas / Ashizawa, Tetsuo / Schut, Lawrence J / Brusco, Alfredo / Berglund, J Andrew / Hasholt, Lis F / Nielsen, Jorgen E / Subramony, S H / Ranum, Laura Pw

    EMBO molecular medicine

    2021  Volume 13, Issue 11, Page(s) e14095

    Abstract: ... and in cell culture experiments, increase p-eIF2α and polyAla and polySer RAN protein levels ... RAN protein levels, polyGln protein toxicity, and disease penetrance and provide novel insight ...

    Abstract Spinocerebellar ataxia type 8 (SCA8), a dominantly inherited neurodegenerative disorder caused by a CTG•CAG expansion, is unusual because most individuals that carry the mutation do not develop ataxia. To understand the variable penetrance of SCA8, we studied the molecular differences between highly penetrant families and more common sporadic cases (82%) using a large cohort of SCA8 families (n = 77). We show that repeat expansion mutations from individuals with multiple affected family members have CCG•CGG interruptions at a higher frequency than sporadic SCA8 cases and that the number of CCG•CGG interruptions correlates with age at onset. At the molecular level, CCG•CGG interruptions increase RNA hairpin stability, and in cell culture experiments, increase p-eIF2α and polyAla and polySer RAN protein levels. Additionally, CCG•CGG interruptions, which encode arginine interruptions in the polyGln frame, increase toxicity of the resulting proteins. In summary, SCA8 CCG•CGG interruptions increase polyAla and polySer RAN protein levels, polyGln protein toxicity, and disease penetrance and provide novel insight into the molecular differences between SCA8 families with high vs. low disease penetrance.
    MeSH term(s) Ataxia ; Humans ; Nerve Tissue Proteins/genetics ; Penetrance ; Proteins ; RNA, Long Noncoding/genetics ; Spinocerebellar Degenerations/genetics ; Trinucleotide Repeat Expansion
    Chemical Substances ATXN8 protein, human ; ATXN8OS gene product, human ; Nerve Tissue Proteins ; Proteins ; RNA, Long Noncoding
    Language English
    Publishing date 2021-10-11
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2467145-9
    ISSN 1757-4684 ; 1757-4676
    ISSN (online) 1757-4684
    ISSN 1757-4676
    DOI 10.15252/emmm.202114095
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Determining the protective effects of Ma-Mu-Ran Antidiarrheal Capsules against acute DSS-induced enteritis using 16S rRNA gene sequencing and fecal metabolomics.

    Zheng, Si-Li / Zhang, Dong-Ning / Duan, Yan-Fen / Huang, Fang / Han, Lin-Tao / Mo, Guo-Yan

    Chinese journal of natural medicines

    2022  Volume 20, Issue 5, Page(s) 364–377

    Abstract: Ma-Mu-Ran Antidiarrheal Capsules (MMRAC) is traditional Chinese medicine that has been used ...

    Abstract Ma-Mu-Ran Antidiarrheal Capsules (MMRAC) is traditional Chinese medicine that has been used to treat diarrhea caused by acute enteritis (AE) and bacillary dysentery in Xinjiang (China) for many years. However, the potential therapeutic mechanism of MMRAC for AE and its regulatory mechanism on host metabolism is unclear. This study used fecal metabolomics profiling with GC/MS and 16S rRNA gene sequencing analysis to explore the potential regulatory mechanisms of MMRAC on a dextran sulfate sodium salt (DSS)-induced mouse model of AE. Fecal metabolomics-based analyses were performed to detect the differentially expressed metabolites and metabolic pathways. The 16S rRNA gene sequencing analysis was used to assess the altered gut microbes at the genus level and for functional prediction. Moreover, Pearson correlation analysis was used to integrate differentially expressed metabolites and altered bacterial genera. The results revealed that six intestinal bacteria and seven metabolites mediated metabolic disorders (i.e., metabolism of amino acid, carbohydrate, cofactors and vitamins, and lipid) in AE mice. Besides, ten altered microbes mediated the differential expression of eight metabolites and regulated these metabolisms after MMRAC administration. Overall, these findings demonstrate that AE is associated with metabolic disorders and microbial dysbiosis. Further, we present that MMRAC exerts protective effects against AE by improving host metabolism through the intestinal flora.
    MeSH term(s) Animals ; Antidiarrheals/pharmacology ; Capsules ; Enteritis/chemically induced ; Enteritis/drug therapy ; Enteritis/genetics ; Feces/microbiology ; Genes, rRNA ; Metabolomics ; Mice ; RNA, Ribosomal, 16S/genetics
    Chemical Substances Antidiarrheals ; Capsules ; RNA, Ribosomal, 16S
    Language English
    Publishing date 2022-05-12
    Publishing country China
    Document type Journal Article
    ZDB-ID 2192577-X
    ISSN 1875-5364 ; 2095-6975 ; 1672-3651
    ISSN (online) 1875-5364
    ISSN 2095-6975 ; 1672-3651
    DOI 10.1016/S1875-5364(22)60158-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: RAN Translation Regulated by Muscleblind Proteins in Myotonic Dystrophy Type 2.

    Zu, Tao / Cleary, John D / Liu, Yuanjing / Bañez-Coronel, Monica / Bubenik, Jodi L / Ayhan, Fatma / Ashizawa, Tetsuo / Xia, Guangbin / Clark, H Brent / Yachnis, Anthony T / Swanson, Maurice S / Ranum, Laura P W

    Neuron

    2017  Volume 95, Issue 6, Page(s) 1292–1305.e5

    Abstract: ... RAN proteins, raising the possibility of a mechanistic connection. We explored this question using ... QAGR) RAN proteins, respectively. In DM2 autopsy brains, LPAC is found in neurons, astrocytes, and glia ... RNAs exceed RBP sequestration capacity, are exported to the cytoplasm, and undergo RAN translation ...

    Abstract Several microsatellite-expansion diseases are characterized by the accumulation of RNA foci and RAN proteins, raising the possibility of a mechanistic connection. We explored this question using myotonic dystrophy type 2, a multisystemic disease thought to be primarily caused by RNA gain-of-function effects. We demonstrate that the DM2 CCTG⋅CAGG expansion expresses sense and antisense tetrapeptide poly-(LPAC) and poly-(QAGR) RAN proteins, respectively. In DM2 autopsy brains, LPAC is found in neurons, astrocytes, and glia in gray matter, and antisense QAGR proteins accumulate within white matter. LPAC and QAGR proteins are toxic to cells independent of RNA gain of function. RNA foci and nuclear sequestration of CCUG transcripts by MBNL1 is inversely correlated with LPAC expression. These data suggest a model that involves nuclear retention of expansion RNAs by RNA-binding proteins (RBPs) and an acute phase in which expansion RNAs exceed RBP sequestration capacity, are exported to the cytoplasm, and undergo RAN translation. VIDEO ABSTRACT.
    MeSH term(s) Brain/metabolism ; Cell Survival ; Cells, Cultured ; Gene Expression Regulation ; Humans ; Mutation ; Myotonic Dystrophy/metabolism ; Protein Biosynthesis ; RNA/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; ran GTP-Binding Protein/biosynthesis ; ran GTP-Binding Protein/toxicity
    Chemical Substances CNBP protein, human ; MBNL1 protein, human ; RNA-Binding Proteins ; RNA (63231-63-0) ; ran GTP-Binding Protein (EC 3.6.5.2)
    Language English
    Publishing date 2017-09-14
    Publishing country United States
    Document type Journal Article ; Video-Audio Media
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2017.08.039
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Antibody Therapy Targeting RAN Proteins Rescues C9 ALS/FTD Phenotypes in C9orf72 Mouse Model.

    Nguyen, Lien / Montrasio, Fabio / Pattamatta, Amrutha / Tusi, Solaleh Khoramian / Bardhi, Olgert / Meyer, Kevin D / Hayes, Lindsey / Nakamura, Katsuya / Banez-Coronel, Monica / Coyne, Alyssa / Guo, Shu / Laboissonniere, Lauren A / Gu, Yuanzheng / Narayanan, Saravanakumar / Smith, Benjamin / Nitsch, Roger M / Kankel, Mark W / Rushe, Mia / Rothstein, Jeffrey /
    Zu, Tao / Grimm, Jan / Ranum, Laura P W

    Neuron

    2019  Volume 105, Issue 4, Page(s) 645–662.e11

    Abstract: ... and antisense-expansion RNAs and six dipeptide repeat-associated, non-ATG (RAN ... RAN proteins. These antibodies cross the blood-brain barrier and co-localize with intracellular RAN aggregates ...

    Abstract The intronic C9orf72 G4C2 expansion, the most common genetic cause of ALS and FTD, produces sense- and antisense-expansion RNAs and six dipeptide repeat-associated, non-ATG (RAN) proteins, but their roles in disease are unclear. We generated high-affinity human antibodies targeting GA or GP RAN proteins. These antibodies cross the blood-brain barrier and co-localize with intracellular RAN aggregates in C9-ALS/FTD BAC mice. In cells, α-GA
    MeSH term(s) Aged ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Animals ; Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/genetics ; Antibodies, Monoclonal/metabolism ; Brain/metabolism ; C9orf72 Protein/genetics ; C9orf72 Protein/metabolism ; Cell Line, Tumor ; Disease Models, Animal ; Female ; Frontotemporal Dementia/genetics ; Frontotemporal Dementia/metabolism ; Gene Targeting/methods ; Genetic Therapy/methods ; HEK293 Cells ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Phenotype ; Random Allocation ; Recombinant Proteins/administration & dosage ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; ran GTP-Binding Protein/antagonists & inhibitors ; ran GTP-Binding Protein/metabolism
    Chemical Substances Antibodies, Monoclonal ; C9orf72 Protein ; C9orf72 protein, mouse ; Ran protein, mouse ; Recombinant Proteins ; ran GTP-Binding Protein (EC 3.6.5.2)
    Language English
    Publishing date 2019-12-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2019.11.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: CCG•CGG interruptions in high‐penetrance SCA8 families increase RAN translation and protein toxicity

    Barbara A Perez / Hannah K Shorrock / Monica Banez‐Coronel / Tao Zu / Lisa EL Romano / Lauren A Laboissonniere / Tammy Reid / Yoshio Ikeda / Kaalak Reddy / Christopher M Gomez / Thomas Bird / Tetsuo Ashizawa / Lawrence J Schut / Alfredo Brusco / J Andrew Berglund / Lis F Hasholt / Jorgen E Nielsen / SH Subramony / Laura PW Ranum

    EMBO Molecular Medicine, Vol 13, Iss 11, Pp n/a-n/a (2021)

    2021  

    Abstract: ... RAN protein levels. Additionally, CCG•CGG interruptions, which encode arginine interruptions in the polyGln ... polyAla and polySer RAN protein levels, polyGln protein toxicity, and disease penetrance and provide novel ...

    Abstract Abstract Spinocerebellar ataxia type 8 (SCA8), a dominantly inherited neurodegenerative disorder caused by a CTG•CAG expansion, is unusual because most individuals that carry the mutation do not develop ataxia. To understand the variable penetrance of SCA8, we studied the molecular differences between highly penetrant families and more common sporadic cases (82%) using a large cohort of SCA8 families (n = 77). We show that repeat expansion mutations from individuals with multiple affected family members have CCG•CGG interruptions at a higher frequency than sporadic SCA8 cases and that the number of CCG•CGG interruptions correlates with age at onset. At the molecular level, CCG•CGG interruptions increase RNA hairpin stability, and in cell culture experiments, increase p‐eIF2α and polyAla and polySer RAN protein levels. Additionally, CCG•CGG interruptions, which encode arginine interruptions in the polyGln frame, increase toxicity of the resulting proteins. In summary, SCA8 CCG•CGG interruptions increase polyAla and polySer RAN protein levels, polyGln protein toxicity, and disease penetrance and provide novel insight into the molecular differences between SCA8 families with high vs. low disease penetrance.
    Keywords cis‐modifier ; RAN translation ; reduced penetrance ; sequence interruptions ; spinocerebellar ataxia type 8 ; Medicine (General) ; R5-920 ; Genetics ; QH426-470
    Language English
    Publishing date 2021-11-01T00:00:00Z
    Publisher Wiley
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: SCA8 RAN polySer protein preferentially accumulates in white matter regions and is regulated by eIF3F.

    Ayhan, Fatma / Perez, Barbara A / Shorrock, Hannah K / Zu, Tao / Banez-Coronel, Monica / Reid, Tammy / Furuya, Hirokazu / Clark, H Brent / Troncoso, Juan C / Ross, Christopher A / Subramony, S H / Ashizawa, Tetsuo / Wang, Eric T / Yachnis, Anthony T / Ranum, Laura Pw

    The EMBO journal

    2018  Volume 37, Issue 19

    Abstract: Spinocerebellar ataxia type 8 (SCA8) is caused by a bidirectionally transcribed CTG·CAG expansion that results in ... ...

    Abstract Spinocerebellar ataxia type 8 (SCA8) is caused by a bidirectionally transcribed CTG·CAG expansion that results in the
    MeSH term(s) Aging/genetics ; Aging/metabolism ; Aging/pathology ; Animals ; Eukaryotic Initiation Factor-3/genetics ; Eukaryotic Initiation Factor-3/metabolism ; HeLa Cells ; Humans ; Mice ; Mice, Transgenic ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Spinocerebellar Degenerations/genetics ; Spinocerebellar Degenerations/metabolism ; Spinocerebellar Degenerations/pathology ; White Matter/metabolism ; White Matter/pathology
    Chemical Substances Eukaryotic Initiation Factor-3 ; Nerve Tissue Proteins
    Language English
    Publishing date 2018-09-11
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 586044-1
    ISSN 1460-2075 ; 0261-4189
    ISSN (online) 1460-2075
    ISSN 0261-4189
    DOI 10.15252/embj.201899023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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