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A network of gene regulatory factors such as transcription factors and microRNAs establish and maintain the gene expression pattern during hematopoiesis. In this network transcription factors regulate each other and are involved in regulatory loops with microRNAs.The microRNA cluster miR-17-92 is lo...
ORGANISM(S): Homo sapiens (Human) 
2021-09-09 | PXD018052 | Pride
Adult beta cells in the pancreas are the sole source of insulin in our body. Beta cell loss or increased demand for insulin, impose metabolic challenges because adult beta cells are generally quiescent and infrequently re-enter the cell division cycle. miR-17-92/106b is a family of proto-oncogene mi...
ORGANISM(S): Mus musculus (Mouse) 
2019-06-17 | PXD012610 | Pride
The synergism between c-MYC and miR-17-19b, a truncated version of the miR-17-92 cluster, is well documented during tumor initiation. However, little is known about miR-17-19b function in established cancers. Here we investigate the role of miR-17-19b in c-MYC-driven lymphomas by integrating SILAC-b...
ORGANISM(S): Mus musculus (Mouse) 
2015-11-06 | PXD002810 | Pride
The miR-17-92 cluster targets mRNAs involved in distinct pathways which either promote or inhibit tumor progression. However, the cellular and molecular mechanisms underlying miR-17~92 cluster mediated pro- or anti- tumorigenic effects has not been studied. In this study, we found that inhibition of...
ORGANISM(S): Mus musculus 
Medulloblastoma is the most common malignant pediatric brain tumor, and mechanisms underlying its development are poorly understood. We identified recurrent amplification of the miR-17/92 polycistron proto-oncogene in 6% of pediatric medulloblastomas by high-resolution single-nucleotide polymorphism...
ORGANISM(S): Homo sapiens 
Gain of chromosome arm 13q is one of the most prevalent DNA copy number alterations associated with colorectal adenoma-to-carcinoma progression. The oncogenic miR-17-92 cluster, located at 13q, was found to be overexpressed in colorectal cancer and in adenomas harboring 13q gain. However, to what ex...
We have generated a miR-17-92 transgenic allele (termed miR-17-92 Tg) whose expression can be turned on conditionally by Cre recombinase (Xiao et al, Nature Immunology, 9:405-14, 2008). The mice were crossed to CD19-Cre mice to turn on the transgene expression specifically in B cells. Follicular B(F...
ORGANISM(S): Mus musculus 
We induced specific deletion of miR-17-92 in Sertoli cells at the time of Amh expression in mouse embryos. We analyzed the effect of this deletion in the long term in adult testis. The transcriptome of mutant testis was consistently altered but do not produce a phenotype due to the testis homeostasi...
ORGANISM(S): Mus musculus 
Methionine COFRADIC combined with Arg and Lys SILAC labeling was used to quantify proteins upon induction of miR-17-92 in SHEP neuroblastoma cells. Differently labeled cells treated with tetracycline for 72 h or left untreated, were harvested and mixed lysates were analyzed by methionine COFRADIC to...
ORGANISM(S): Homo sapiens (Human) 
2010-12-10 | PRD000321 | Pride
Purpose: The goal of this study is to compare the differential expression of transcripts in control kidneys compared to kidneys lacking the miR-17~92 cluster in nephron progenitors and their derivatives by RNA-seq to identify potential miRNA targets in the mutant kidneys. mRNA profiles of control an...
ORGANISM(S): Mus musculus 
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