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    CUL7 cullin 7 [ Homo sapiens (human) ]

    Gene ID: 9820, updated on 7-Oct-2018

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Study shows that cullin 7 is highly expressed in breast cancer cells and suggests that positive expression is associated with the malignant phenotype and a predictor of poor prognosis. Cullin 7 is involved in cell proliferation and invasion by regulating the cell cycle and microtubule stability.

    Cullin 7 is a predictor of poor prognosis in breast cancer patients and is involved in the proliferation and invasion of breast cancer cells by regulating the cell cycle and microtubule stability.
    Qiu N, He Y, Zhang S, Hu X, Chen M, Li H.

    CUL7 expression was associated with EC progression and poor prognosis. CUL7 may promote EMT via the ERKSNAI2 pathway in EC.

    Cullin7 promotes epithelial‑mesenchymal transition of esophageal carcinoma via the ERK‑SNAI2 signaling pathway.
    Tian P, Liu D, Sun L, Sun H.

    overexpression of Cullin7 plays an important role in the pathogenesis and progression of hepatocellular carcinoma and may be a valuable marker for hepatocellular carcinoma management.

    Overexpression of Cullin7 is associated with hepatocellular carcinoma progression and pathogenesis.
    An J, Zhang Z, Liu Z, Wang R, Hui D, Jin Y., Free PMC Article

    Hepatocellular carcinoma patients with positive expression for both Rabl3 and Cullin7 had a remarkably shorter survival time compared with patients with negative expression for both proteins.

    Overexpression of Rabl3 and Cullin7 is associated with pathogenesis and poor prognosis in hepatocellular carcinoma.
    An J, Liu Z, Liang Q, Pan Y, Li H, Wang R, Jin Y.

    our study provided evidence that Cullin7 functions as a novel oncogene in lung cancer and may be a potential therapeutic target for lung cancer management.

    Cullin7 is required for lung cancer cell proliferation and is overexpressed in lung cancer.
    Men X, Wang L, Yu W, Ju Y.

    Cullin7 promotes epithelial-mesenchymal transformation of cancer cells.

    Inhibition of Liver Carcinoma Cell Invasion and Metastasis by Knockdown of Cullin7 In Vitro and In Vivo.
    Zhang D, Yang G, Li X, Xu C, Ge H.

    We report a family with variable phenotypic features of 3-M syndrome and we describe the prenatal and postnatal growth pattern of two affected sisters with a novel homozygous CUL7 mutation (c.3173-1G>C), showing a pre- and post-natal growth deficiency and a normal cranial circumference.

    Pre- and post-natal growth in two sisters with 3-M syndrome.
    Lugli L, Bertucci E, Mazza V, Elmakky A, Ferrari F, Neuhaus C, Percesepe A.

    report an adult female with 3-M syndrome that was caused by novel compound heterozygous mutations (c.4023-1 G>A in splice acceptor site of exon 22 and c.4359_4363dupGGCTG in exon 23) in the CUL7 gene

    Changes in facial appearance from neonate to adult in 3-M syndrome patient with novel CUL7 gene mutations.
    Hasegawa K, Tanaka H, Higuchi Y, Yamashita M, Tsukahara H.

    Cullin7 may serve as an indicator of poor prognosis in patients with epithelial ovarian cancer.

    High Expression of Cullin7 Correlates with Unfavorable Prognosis in Epithelial Ovarian Cancer Patients.
    Xi J, Zeng ST, Guo L, Feng J.

    study provided evidence that Cullin7 functions as a novel oncogene in breast cancer and may be a potential therapeutic target for breast cancer management

    Overexpressed ubiquitin ligase Cullin7 in breast cancer promotes cell proliferation and invasion via down-regulating p53.
    Guo H, Wu F, Wang Y, Yan C, Su W.

    CUL7, OBSL1 and CCDC8 modulate the alternative splicing of the INSR

    Identifying biological pathways that underlie primordial short stature using network analysis.
    Hanson D, Stevens A, Murray PG, Black GC, Clayton PE., Free PMC Article

    The CUL7, OBSL1, and CCDC8 proteins form a 3M complex that functions in maintaining microtubule and genome integrity and normal development.

    The 3M complex maintains microtubule and genome integrity.
    Yan J, Yan F, Li Z, Sinnott B, Cappell KM, Yu Y, Mo J, Duncan JA, Chen X, Cormier-Daire V, Whitehurst AW, Xiong Y., Free PMC Article

    CUL7/Fbxw8 ubiquitin ligase-mediated HPK1 degradation revealed a direct link and novel role of CUL7/Fbxw8 ubiquitin ligase in the MAPK pathway, which plays a critical role in cell proliferation and differentiation.

    The CUL7/F-box and WD repeat domain containing 8 (CUL7/Fbxw8) ubiquitin ligase promotes degradation of hematopoietic progenitor kinase 1.
    Wang H, Chen Y, Lin P, Li L, Zhou G, Liu G, Logsdon C, Jin J, Abbruzzese JL, Tan TH, Wang H., Free PMC Article

    Homozygous deletion in exon 18 of the CUL7 gene, which has not been previously described, could be responsible for the 3-M syndrome.

    3-M syndrome associated with growth hormone deficiency: 18 year follow-up of a patient.
    Meazza C, Lausch E, Pagani S, Bozzola E, Calcaterra V, Superti-Furga A, Silengo M, Bozzola M., Free PMC Article

    This study demonstrates specific genomic alterations in HCC/MS and points to CUL7 as a novel gene potentially involved in liver carcinogenesis associated with metabolic Syndrome, the amplification of which might influence cell proliferation.

    Cullin7: a new gene involved in liver carcinogenesis related to metabolic syndrome.
    Paradis V, Albuquerque M, Mebarki M, Hernandez L, Zalinski S, Quentin S, Belghiti J, Soulier J, Bedossa P.

    Dysregulation of Cul7 and Fbxw8 expression might affect trophoblast turnover in intrauterine growth restriction.

    Cullin 7 and Fbxw 8 expression in trophoblastic cells is regulated via oxygen tension: implications for intrauterine growth restriction?
    Fahlbusch FB, Dawood Y, Hartner A, Menendez-Castro C, Nögel SC, Tzschoppe A, Schneider H, Strissel P, Beckmann MW, Schleussner E, Ruebner M, Dörr HG, Schild RL, Rascher W, Dötsch J.

    Mutations in CUL7, OBSL1 and CCDC8 in 3-M syndrome lead to disordered growth factor signalling.

    Mutations in CUL7, OBSL1 and CCDC8 in 3-M syndrome lead to disordered growth factor signalling.
    Hanson D, Murray PG, Coulson T, Sud A, Omokanye A, Stratta E, Sakhinia F, Bonshek C, Wilson LC, Wakeling E, Temtamy SA, Aglan M, Rosser EM, Mansour S, Carcavilla A, Nampoothiri S, Khan WI, Banerjee I, Chandler KE, Black GC, Clayton PE.

    Growth factor-stimulated TBC1D3 ubiquitination and degradation are regulated by its interaction with CUL7-Fbw8.

    Ubiquitination and degradation of the hominoid-specific oncoprotein TBC1D3 is mediated by CUL7 E3 ligase.
    Kong C, Samovski D, Srikanth P, Wainszelbaum MJ, Charron AJ, Liu J, Lange JJ, Chen PI, Pan ZQ, Su X, Stahl PD., Free PMC Article

    discussion of roles of CUL7, OBSL1 (obscurin-like 1), and CCDC8 (coiled-coil domain containing protein 8) in growth and development using findings from patients with Miller-McKusick-Malvaux syndrome and Silver-Russell syndrome [REVIEW]

    The genetics of 3-M syndrome: unravelling a potential new regulatory growth pathway.
    Hanson D, Murray PG, Black GC, Clayton PE.

    binding of Cul1-Rbx1 to Cul7-Rbx1 is mediated via heterodimerization of Fbxw8 with other F-box proteins which function to recruit substrates into the E3 ligase complex

    Characterization of the Cullin7 E3 ubiquitin ligase--heterodimerization of cullin substrate receptors as a novel mechanism to regulate cullin E3 ligase activity.
    Ponyeam W, Hagen T.

    We propose that CUL7, OBSL1, and CCDC8 are members of a pathway controlling mammalian growth.

    Exome sequencing identifies CCDC8 mutations in 3-M syndrome, suggesting that CCDC8 contributes in a pathway with CUL7 and OBSL1 to control human growth.
    Hanson D, Murray PG, O'Sullivan J, Urquhart J, Daly S, Bhaskar SS, Biesecker LG, Skae M, Smith C, Cole T, Kirk J, Chandler K, Kingston H, Donnai D, Clayton PE, Black GC., Free PMC Article

    CUL7 appears to be the major gene responsible for 3M syndrome accounting for 77.5% of cases while OBSL1 mutations accounts for 16.3%[review]

    The 3M syndrome.
    Huber C, Munnich A, Cormier-Daire V.

    CUL7 expression in placenta is up-regulated up to 10 times in intra-uterine growth restriction (IUGR) and up to 15 times in preeclampsia associated with IUGR; the CUL7 promoter is hypomethylated in IUGR.

    Cullins in human intra-uterine growth restriction: expressional and epigenetic alterations.
    Gascoin-Lachambre G, Buffat C, Rebourcet R, Chelbi ST, Rigourd V, Mondon F, Mignot TM, Legras E, Simeoni U, Vaiman D, Barbaux S.

    in 33 novel cases of 3M syndrome, we identified deleterious CUL7 mutations in 23/33 patients, including 19 novel mutations & 1 paternal isodisomy of chromosome 6 encompassing a CUL7 mutation; findings also support genetic heterogeneity of this disease

    A large-scale mutation search reveals genetic heterogeneity in 3M syndrome.
    Huber C, Delezoide AL, Guimiot F, Baumann C, Malan V, Le Merrer M, Da Silva DB, Bonneau D, Chatelain P, Chu C, Clark R, Cox H, Edery P, Edouard T, Fano V, Gibson K, Gillessen-Kaesbach G, Giovannucci-Uzielli ML, Graul-Neumann LM, van Hagen JM, van Hest L, Horovitz D, Melki J, Partsch CJ, Plauchu H, Rajab A, Rossi M, Sillence D, Steichen-Gersdorf E, Stewart H, Unger S, Zenker M, Munnich A, Cormier-Daire V., Free PMC Article

    A novel homozygous 4582insT mutation in CUL7 resulted in a frameshift mutation & a premature stop codon at 1553 (Q1553X)in Yakuts with short stature syndromes.

    Clinical, molecular and histopathological features of short stature syndrome with novel CUL7 mutation in Yakuts: new population isolate in Asia.
    Maksimova N, Hara K, Miyashia A, Nikolaeva I, Shiga A, Nogovicina A, Sukhomyasova A, Argunov V, Shvedova A, Ikeuchi T, Nishizawa M, Kuwano R, Onodera O., Free PMC Article

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