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Find video protocols related to scientific articles indexed in Pubmed.
A recessive variant of XRCC4 predisposes to non- BRCA1/2 breast cancer in chinese women and impairs the DNA damage response via dysregulated nuclear localization.
Oncotarget
PUBLISHED: 09-07-2014
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XRCC4 plays a crucial role in the non-homologous end joining pathway that maintains genome stability. In this two-stage case-control study with 1,764 non-BRCA1/2 breast cancer patients and 1,623 cancer-free controls, we investigated the contribution of genetic variants of XRCC4 to breast cancer susceptibility in Chinese women. We identified a recessive missense variant, rs3734091 (c.739G>T, p.Ala247Ser), of XRCC4 that was significantly associated with an increased risk of breast cancer (odds ratio [OR] = 3.92, P = 0.007), particularly with the risk of developing triple-negative breast cancer (OR = 18.65, P < 0.0001). This p.Ala247Ser variant disturbed the nuclear localization of XRCC4 in cells homozygous for the rs3734091-T allele but not in heterozygous cells at both the cellular and tissue levels. In heterozygous cells, wild-type XRCC4 facilitated the nuclear localization of the XRCC4A247S mutant, thus compensating for the impaired localization of XRCC4A247S. This provided a biological mechanism by which rs3734091 conferred an increased susceptibility to non-BRCA1/2 breast cancer exclusively under a recessive model. Further functional analyses revealed that p.Ala247Ser impaired the DNA damage repair capacity and ultimately perturbed genomic stability. Taken together, our findings document the role of XRCC4 in non-BRCA1/2 breast cancer predisposition and reveal its underlying biological mechanism of action.
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ID2 predicts poor prognosis in breast cancer, especially in triple-negative breast cancer, and inhibits E-cadherin expression.
Onco Targets Ther
PUBLISHED: 01-01-2014
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Inhibitors of DNA-binding (ID) proteins are known as important modulators in the regulation of cell proliferation and differentiation. This study sought to investigate the prognostic value of ID proteins in breast cancer.
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[Effects of bisphenol A on OCT4 and SOX2 genes expression in mouse embryonic stem cells].
Zhonghua Yu Fang Yi Xue Za Zhi
PUBLISHED: 05-31-2013
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To explore the effects of bisphenol A (BPA) exposure on toxicity characteristic and OCT4 and SOX2 gene expression of mouse embryonic stem cells (mESC).
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MicroRNA-200a promotes anoikis resistance and metastasis by targeting YAP1 in human breast cancer.
Clin. Cancer Res.
PUBLISHED: 01-22-2013
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The process of metastases involves the dissociation of cells from the primary tumor, penetration into the basement membrane, invasion, and exiting from the vasculature to seed and colonize distant tissues. miR-200a is involved in this multistep metastatic cascade. This study aimed to test the hypothesis that miR-200a promotes metastasis through increased anoikis resistance in breast cancer.
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Nogo receptor 3, a paralog of Nogo-66 receptor 1 (NgR1), may function as a NgR1 co-receptor for Nogo-66.
J Genet Genomics
PUBLISHED: 08-15-2011
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Nogo-A is a major myelin associated inhibitor that blocks regeneration of injured axons in the central nervous system (CNS). Nogo-66 (a 66-residue domain of Nogo-A) expressed on the surface of oligodendrocytes has been shown to directly interact with Nogo-66 receptor 1 (NgR1). A number of additional components of NgR1 receptor complex essential for its signaling have been uncovered. However, detailed composition of the complex and its signaling mechanisms remain to be fully elucidated. In this study, we show that Nogo receptor 3 (NgR3), a paralog of NgR1, is a binding protein for NgR1. The interaction is highly specific because other members of the reticulin family, to which Nogo-A belongs, do not bind to NgR3. Neither does NgR3 show any binding activity with Nogo receptor 2 (NgR2), another NgR1 paralog. Majority of NgR3 domains are required for its binding to NgR1. Moreover, a truncated NgR3 with the membrane anchoring domain deleted can function as a decoy receptor to reverse neurite outgrowth inhibition caused by Nogo-66 in culture. These in vitro results, together with previously reported overlapping expression profile between NgR1 and NgR3, suggest that NgR3 may be associated with NgR1 in vivo and that their binding interface may be targeted for treating neuronal injuries.
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Reprogramming of mouse and human somatic cells by high-performance engineered factors.
EMBO Rep.
PUBLISHED: 01-15-2011
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Reprogramming somatic cells to become induced pluripotent stem cells (iPSCs) by using defined factors represents an important breakthrough in biology and medicine, yet remains inefficient and poorly understood. We therefore devised synthetic factors by fusing the VP16 transactivation domain to OCT4 (also known as Pou5f1), NANOG and SOX2, respectively. These synthetic factors could reprogramme both mouse and human fibroblasts with enhanced efficiency and accelerated kinetics. Remarkably, Oct4-VP16 alone could efficiently reprogramme mouse embryonic fibroblasts (MEFs) into germline-competent iPSCs. Furthermore, episomally delivered synthetic factors could reproducibly generate integration-free iPSCs from MEFs with enhanced efficiency. Our results not only demonstrate the feasibility of engineering more potent reprogramming factors, but also suggest that transcriptional reactivation of OCT4 target genes might be a rate-limiting step in the conversion of somatic cells to pluripotent cells. Synthetic factor-based reprogramming might lead to a paradigm shift in reprogramming research.
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Principles of hatchet-skin flap for repair of tissue defects on the cheek.
Aesthetic Plast Surg
PUBLISHED: 01-12-2011
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To date, cheek reconstruction remains a challenge for plastic surgeons. This report presents the authors cheek reconstruction technique with different types of hatchet-skin flaps, which provides satisfactory results.
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[Application principles of hatchet skin flap for repairing tissue defect of cheek].
Zhonghua Wai Ke Za Zhi
PUBLISHED: 11-09-2010
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To evaluate the design principles, clinical results and significance of hatchet skin flaps for repairing tissue defects in different parts of cheek.
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[Effect of the tumescent infiltration solution temperature on body temperature].
Zhonghua Zheng Xing Wai Ke Za Zhi
PUBLISHED: 11-05-2010
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To evaluate the effect of tumescent infiltration solution temperature on core body temperature after liposuction.
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[Application of hatchet flap for buccal tissue defect].
Zhonghua Zheng Xing Wai Ke Za Zhi
PUBLISHED: 12-25-2009
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To evaluate the therapeutic effect of hatchet flap for buccal tissue defect.
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Activity of long-chain acyl-CoA synthetase is required for maintaining meiotic arrest in Xenopus laevis.
Biol. Reprod.
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In most vertebrates, fully grown oocytes are arrested in meiotic prophase I and only resume the cell cycle upon external stimuli, such as hormones. The proper arrest and resumption of the meiotic cycle is critical for reproduction. A Galpha(S) signaling pathway essential for the arrest is conserved in organisms from Xenopus to mouse and human. A previous gene association study implicated that mutations of human ACSL6 may be related to premature ovarian failure. However, functional roles of ACSL6 in human infertility have yet to be reported. In the present study, we found that triacsin C, a potent and specific inhibitor for ACSL, triggers maturation in Xenopus and mouse oocytes in the absence of hormone, suggesting ACSL activity is required for the oocyte arrest. In Xenopus, acsl1b may fulfill a major role in the process, because inhibition of acsl1b by knocking down its RNA results in abnormal acceleration of oocyte maturation. Such abnormally matured eggs cannot support early embryonic development. Moreover, direct inhibition of protein palmitoylation, which lies downstream of ACSLs, also causes oocyte maturation. Furthermore, palmitoylation of Galpha(s), which is essential for its function, is inhibited when the ACSL activity is blocked by triacsin C in Xenopus. Thus, disruption of ACSL activity causes inhibition of the Galpha(s) signaling pathway in the oocytes, which may result in premature ovarian failure in human.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

How does it work?

We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.