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In the current study, we show a new role of miR-17-92 in inhibiting oncogenic ras -induced senescence. The miR-17-92 cluster is also crucial in the development of B-NHL. Tagawa et al documented that c-Myc can not only promote the transcription of miR-17-92 cluster, but can also act as a target of the miR-17-92 cluster. A high-level of miR-17-92 cluster expression also results in the poor survival rate of patients with MCL . Interestingly, deletion or overexpression of miR-17- 92 cluster in keratinocytes, or deletion of miR-17-92 in T cells did not significantly affect IMQ-induced psoriasis- like dermatitis develop-ment in the mutant mice compared with wild-type littermates. Thus, miRNA miR-17- 92 cluster Members of the miRNA gene cluster can coordinate the regulation of certain processes or play a similar role in the same biological process, ensuring biological activity occurs in a normal and orderly fashion.
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The miR-17-92 gene cluster, a polycistron encoding six microRNAs (miRNA), is frequ … In mammalian cells, activation of oncogenes usually triggers innate tumor-suppressing defense mechanisms, including apoptosis and senescence, which are compromised by additional mutations before cancers are developed. 3. Expression and regulation of the miRNA-17-92 cluster in tumor cells Expression and functions of miR-17/20a. The miRNA-17-92 cluster may be highly expressed in a wide range of tumor cells and types of cancer, such as lung, breast, pancreatic, prostate and thyroid cancer, as well as lymphomas (7,14). Therefore, it is also referred to as MiR-17-92 cluster is an oncogenic miRNA cluster that is implicated in several cancers, although its role in hepatocarcinogenesis has not been clearly defined. In this study, we show that the miR-17-92 cluster is highly expressed in human hepatocellular carcinoma (HCC) tissues compared to the non-tumorous liver tissues by RT-PCR and in situ hybridization analyses. In humans, the activating mutations of miR-17~92 have been identified in non-Hodgkin's lymphoma, whereas the miRNA constituents of the clusters are overexpressed in a multiple cancer types.
Thus, miRNA miR-17- 92 cluster Members of the miRNA gene cluster can coordinate the regulation of certain processes or play a similar role in the same biological process, ensuring biological activity occurs in a normal and orderly fashion. miR-17-92 encodes a miRNA precursor and produces 7 mature miRNA molecules that belong to 4 miRNA families. To investigate whether this miRNA panel might be used as a non-invasive biomarker, miR-17/92 cluster expression profile was analyzed in peripheral blood.
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Here,we show that miR-17~92, an oncogenic miRNA cluster, is up-regulated in mouse models of PKD. Kidney-specific transgenic overexpression of miR-17~92 produces kidney cysts in mice. miRNA miR‐17‐92 cluster is differentially regulated in the imiqumod‐treated skin but is not required for imiqumod‐induced psoriasis‐like dermatitis in mice Dinghong Wu Department of Dermatology, Guangdong provincial Hospital of Chinese Medicine, Guanghzou, China that the miR-17-92 cluster regulates adult neurogenesis in the subventricular zone (SVZ) (12). However, the in vivo effect of the miR-17-92 cluster on adult neurogenesis in the hippocampus and consequent neurobehavioral function, especially learning and memory, has not been investigated.
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The miRNA expression profiles of THY1-enriched undifferentiated spermatogonia were characterized, and members of Mir-17-92 (Mirc1) and its paralog Mir-106b-25 (Mirc3) clusters are significantly downregulated during retinoic acid-induced spermatogonial differentiation, both in vitro and in vivo. The miR-17-92 cluster is often amplified or overexpressed in human cancers and has recently emerged as the prototypical oncogenic polycistron miRNA.
We successfully integrated exogenous shRNAs at the porcine miRNA-17-92 (pmiR-17-92) cluster via a CRISPR/Cas9-mediated knock-in strategy. We dissected the role of individual miRNA components of the miR-17-92 cluster in thyroid differentiation, especially the impact on NIS levels, and observed that while some miRNAs such as miR-17-5p, miR-19a/b, and miR-92 may inhibit NIS expression, others such as miR-20a-5p do not modulate NIS levels. 2013-11-11 · MiR-17/92 is one of the best-known miRNA clusters.
Research work in recent years has revealed unexpected roles of miRNA-17-92 cluster due to its members have function in a wide variety of settings that include normal development, immune diseases, cardiovascular diseases, neurodegenerative diseases and aging. Signosis has developed miR-17-92 cluster real-time PCR kit to detect the expression of 2020-06-17 2013-11-11 · MiR-17/92 is one of the best-known miRNA clusters. The cluster’s members have pivotal roles in normal development, and dysregulation of their expression leads to a wide array of diseases MiR-17-92 cluster is an oncogenic miRNA cluster that is implicated in several cancers, although its role in hepatocarcinogenesis has not been clearly defined. In this study, we show that the miR-17-92 cluster is highly expressed in human hepatocellular carcinoma (HCC) tissues compared to the non-tumorous liver tissues by RT-PCR and in situ hybridization analyses. The mircoRNA-17-92 cluster encoded by the miR-17-92 host gene is first found in malignant B-cell lymphoma.
Tagawa et al documented that c-Myc can not only promote the transcription of miR-17-92 cluster, but can also act as a target of the miR-17-92 cluster.
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Its transcription is in part controlled by an E2F-regulated host gene promoter. An intronic A/T-rich region directly upstream of the miRNA coding region also contributes to cluster expression.
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Olive et al. (2009) approached the dissection of the miR-17-92 cluster from the opposite side, by overexpression of different miRNA components in the Eμ-Myc-induced B-cell lymphomas. They found that overexpression of the entire cluster, the cluster without miR-92, but not when miR-19a and miR-19b were lost, enhanced oncogenesis. The miR-17-92 cluster is often amplified or overexpressed in human cancers and has recently emerged as the prototypical oncogenic polycistron miRNA. The functional analysis of miR-17-92 is intricate by the existence of two paralogues: miR-106a-363 and miR-106b-25. This miRNA dose-dependent target selection was also confirmed in other target genes, including CCND1, CDKN1 and E2F1. After overexpressing let-7a-7f or the miR-17-92 clusters at wide-ranging doses, the target genes displayed a nonlinear correlation to the transfected miRNA.
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Patel V (1), Williams D, Hajarnis S, Hunter R, Pontoglio M, Somlo S, Igarashi P. BACKGROUND: MiR-17-92 cluster is coded by MIR17HG in chromosome 13, which is highly conserved in vertebrates. Published literatures have proved that miR-17-92 cluster critically regulates tumorigenesis and metastasis. Recent researches showed that the miR-17-92 cluster also plays novel functions in the endocrine The miR-17-92 cluster (encoding miR-17, -18a, -19a/b, -20a, and miR-92a) is highly expressed in tumor cells and is up-regulated by ischemia. Whereas miR-92a was recently identified as negative regulator of angiogenesis, the specific functions of the other members of the cluster are less clear. A polycistronic microRNA cluster, miR-17–92, is overexpressed in human lung cancers and enhances cell proliferation Cancer Res , 65 ( 2005 ) , pp. 9628 - 9632 View Record in Scopus Google Scholar The miR-17-92 cluster is a typical highly conserved polycistronic miRNA cluster, which is located in the human chromosome 13 open reading frame 25 (C13orf25), encoding six mature miRNAs, including miR-17, miR-18a, miR-19a, miR-19b, miR-20a and miR-92a (10).