Transcripts Targeted by the MicroRNA-16 Family Cooperatively Regulate Cell Cycle Progression

By Peter S. Linsley, Janell M. Schelter, J. Burchard, M. Kibukawa, Melissa M. Martin, S. Bartz, Jason M. Johnson, Jordan M. Cummins, C. Raymond, Hongyue Dai and 5 more. Molecular and Cellular Biology, 2007

600 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ea281daec8dffee8bf0f2d1500d81c6cf4eb3e34

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

In Molecular Biology

Citations in the corpus

The biochemical basis of microRNA targeting efficacy (2018, methodology): “To examine how well our models generalized to another cell type and to a miRNA family not used for fitting (let-7), we evaluated them on repression data collected after transfecting let-7c into HCT116 (human colon cancer) cells that had been engineered to not express endogenous miRNAs (37).”
MicroRNAs: key players in the immune system, differentiation, tumorigenesis and cell death (2008, background): “…in CLL patients Pro-apoptotic effects mediated through BCL2 BCL2 and NGN3a Calin et al. (2005); Cimmino et al. (2005); Joglekar et al. (2007); Linsley et al. (2007) miR-21 Widely overexpressed in cancer; promotes growth; shown to induce a metastatic phenotype Shown to inhibit apoptosis PTEN,…”
The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia. (2010, background): “miR-15a/16-1 Control Proliferation in Mouse and Human B Cells To understand the mechanism by which the deletions lead to clonal B-lymphoproliferations, we investigated whether miR15a/16-1-deletions could affect proliferation of mouse B cells, as previously suggested for nonlymphoid cells (Bandi et a”
Mechanisms of post-transcriptional regulation by microRNAs: are the answers in sight? (2008, background): “, or in which miRNA levels were experimentally altere”
MiR-15a and miR-16-1 cluster functions in human leukemia (2008, background): “Accordingly, we found that some of the described miR-16 targets whose disruption triggered G0/G1-cell accumulation were down-regulated also in our cell model (CDK6, CDC27, RAB11FIP2) and that some of the previously described GO categories [namely ‘‘mitotic cell cycle’’ (GO:278), and ‘‘cell cycle’’ (”
MicroRNAs in development and disease. (2011, background): “In agreement, overexpression of miR-16 inhibits cell proliferation (373) and suppresses tumor growth after in vivo implantation (66).”
MicroRNA: Biogenesis, Function and Role in Cancer (2010, background): “Computer algorithms and proteomic analysis predict a variety of targets linked to cell growth, cell cycle and apoptosis [267, 273].”
Role of microRNAs in vascular diseases, inflammation, and angiogenesis. (2008, background): “Thus, miR-15 and miR-16 induce apoptosis of leukaemic cells by targeting the anti-apoptotic protein Bcl-2, block cell cycle progression and are frequently downregulated in chronic lymphocytic leukaemia.(57,58) In summary, the identification of miRNAs with a dual antitumour and anti-angiogenic effect”
MicroRNA 21 Promotes Glioma Invasion by Targeting Matrix Metalloproteinase Regulators (2008, methodology): “The analysis was performed on RNA samples harvested at 6 and 24 hours posttransfection, consistent with the time frames commonly used for this type of analysis (18, 36, 37).”
Desperately seeking microRNA targets (2010, methodology): “Although this method cannot distinguish direct from indirect targets, harvesting cells soon after transfection might enhance the proportion of direct target”