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    NUS1 NUS1 dehydrodolichyl diphosphate synthase subunit [ Homo sapiens (human) ]

    Gene ID: 116150, updated on 5-Mar-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    These findings provide new insights for understanding the roles of NgBR in regulating breast epithelial cell transform during the pathogenesis of breast cancer.

    Comprehensive proteome quantification reveals NgBR as a new regulator for epithelial-mesenchymal transition of breast tumor cells.
    Zhao B, Xu B, Hu W, Song C, Wang F, Liu Z, Ye M, Zou H, Miao QR., Free PMC Article

    08/15/2015
    Described is a family with a congenital disorder of glycosylation caused by a loss of function mutation in the conserved C terminus of Nogo-B receptor - R290H.

    Mutation of Nogo-B receptor, a subunit of cis-prenyltransferase, causes a congenital disorder of glycosylation.
    Park EJ, Grabińska KA, Guan Z, Stránecký V, Hartmannová H, Hodaňová K, Barešová V, Sovová J, Jozsef L, Ondrušková N, Hansíková H, Honzík T, Zeman J, Hůlková H, Wen R, Kmoch S, Sessa WC., Free PMC Article

    05/23/2015
    Significant NgBR mRNA down-regulation was associated with larger primary tumor size (p=0.039), lymph node involvement (p=0.039) and advancement stage (p=0.0054).

    Expression of Nogo isoforms and Nogo-B receptor (NgBR) in non-small cell lung carcinomas.
    Pula B, Werynska B, Olbromski M, Muszczynska-Bernhard B, Chabowski M, Janczak D, Zabel M, Podhorska-Okolow M, Dziegiel P.

    11/22/2014
    Nogo-B receptor expression correlates negatively with malignancy grade and ki-67 antigen expression in invasive ductal breast carcinoma.

    Nogo-B receptor expression correlates negatively with malignancy grade and ki-67 antigen expression in invasive ductal breast carcinoma.
    Pula B, Olbromski M, Owczarek T, Ambicka A, Witkiewicz W, Ugorski M, Rys J, Zabel M, Dziegiel P, Podhorska-Okolow M.

    11/22/2014
    Nogo-B receptor mediates pulmonary endothelial cell angiogenesis response through Akt/endothelial nitric oxide synthase pathway.

    Nogo-B receptor modulates angiogenesis response of pulmonary artery endothelial cells through eNOS coupling.
    Teng RJ, Rana U, Afolayan AJ, Zhao B, Miao QR, Konduri GG., Free PMC Article

    10/4/2014
    NgBR is a new molecular marker for breast cancer.

    Expression of NgBR is highly associated with estrogen receptor alpha and survivin in breast cancer.
    Wang B, Zhao B, North P, Kong A, Huang J, Miao QR., Free PMC Article

    08/23/2014
    Nogo-B receptor (NgBR) is an essential component of the dolichol monophosophate (Dol-P) biosynthetic machinery. Loss of NgBR results in a robust deficit in cis-isoprenyltransferase (IPTase) activity and Dol-P production.

    Nogo-B receptor is necessary for cellular dolichol biosynthesis and protein N-glycosylation.
    Harrison KD, Park EJ, Gao N, Kuo A, Rush JS, Waechter CJ, Lehrman MA, Sessa WC., Free PMC Article

    08/13/2011
    The Nogo-B receptor localizes primarily to the endoplasmic reticulum and regulates the stability of nascent Niemann-Pick type C2 protein.

    Nogo-B receptor stabilizes Niemann-Pick type C2 protein and regulates intracellular cholesterol trafficking.
    Harrison KD, Miao RQ, Fernandez-Hernándo C, Suárez Y, Dávalos A, Sessa WC., Free PMC Article

    01/21/2010
    In s-IBM muscle the Nogo-B increase may represent an attempt by muscle fiber to decrease A beta production. However, the increase of Nogo-B seems insufficient because A beta continues to accumulate and the disease progresses.

    NOGO is increased and binds to BACE1 in sporadic inclusion-body myositis and in A beta PP-overexpressing cultured human muscle fibers.
    Wojcik S, Engel WK, Yan R, McFerrin J, Askanas V.

    01/21/2010
    identify a previously uncharacterized Nogo-B receptor specific for the amino terminus of Nogo-B

    Identification of a receptor necessary for Nogo-B stimulated chemotaxis and morphogenesis of endothelial cells.
    Miao RQ, Gao Y, Harrison KD, Prendergast J, Acevedo LM, Yu J, Hu F, Strittmatter SM, Sessa WC., Free PMC Article

    01/21/2010
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