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At least 1,243 records · Page 69Linked to original sources
PubMed2002

Control of developmental timing by small temporal RNAs: a paradigm for RNA-mediated regulation of gene expression.

Heterochronic genes control the timing of developmental programs. In C. elegans, two key genes in the heterochronic pathway, lin-4 and let-7, encode small temporally expressed RNAs (stRNAs) that are not translated into protein. These stRNAs exert negative post-transcriptional regulation by binding to complementary sequences in the 3' untranslated regions of their target genes. stRNAs are transcribed as longer precursor RNAs that are processed by the RNase Dicer/DCR-1 and members of the RDE-1/AGO1 family of proteins, which are better known for their roles in RNA interference (RNAi). However, stRNA function appears unrelated to RNAi. Both sequence and temporal regulation of let-7 stRNA is conserved in other animal species suggesting that this is an evolutionarily ancient gene. Indeed, C. elegans, Drosophila and humans encode at least 86 other RNAs with similar structural features to lin-4 and let-7. We postulate that other small non-coding RNAs may function as stRNAs to control temporal identity during development in C. elegans and other organisms.

3' Untranslated Regions↗
PubMed2006

"Mir"acles in hox gene regulation.

Micro RNAs (miRNAs) have been shown to control many cellular processes including developmental timing in different organisms. The prediction that miRNAs are involved in regulating hox genes of flies and mouse is quite a recent idea and is supported by the finding that mir-196 represses Hoxb8 gene expression. The non-coding regions that encode these miRNAs are also conserved across species in the same way as other mechanisms that regulate expression of hox genes. On the contrary, until now no homeotic phenotype, a hallmark of any hox gene mutation, had been associated with any hox miRNA. Recent work on bithorax complex miRNA (miR-iab-4-5p) shows, for the first time, that miRNAs can lead to homeotic transformation. This miRNA regulates Ultrabithorax (Ubx) and results in the transformation of haltere to wing. This study unveils a new complexity and finesse to the regulation of hox gene expression pattern that is needed for determining the anteroposterior body axis in all bilaterians.

Animals↗
PubMed2007

Real time PCR profiling of 330 human micro-RNAs.

The small size of miRNAs makes profiling of all the 462 known human miRNAs difficult using single cell samples. Recently, we showed that judicious sequence partitioning between RT primers and second strand synthesis primers permitted multiplexed RT-PCR amplification of miRNA in very small samples to allow individual real time PCR quantification. Here, we show that zip coding the primers and TaqMan probes with sequences specific to each miRNA greatly improves reaction specificity, which permits the profiling of all miRNAs in a single multiplexed RT-PCR reaction.

Base Sequence↗
PubMed2005

Analysis of the regulation of lin-41 during chick and mouse limb development.

We have cloned the chicken and mouse orthologues of the Caenorhabditis elegans heterochronic gene lin-41. During limb development, lin-41 is expressed in three phases over developmental time and most notably is associated with the developing autopod. Using chicken and mouse mutants and bead implantations, we report that lin-41 is genetically and biochemically downstream of both the Shh and Fgf signaling pathways. In C. elegans, it is proposed that lin-41 activity is temporally regulated by miRNAs (let-7 and lin-4) that bind to complementary sites in the lin-41 3'-untranslated region (UTR). Taking a bioinformatics approach, we also report the presence of potential miRNA binding sites in the 3'-UTR of chicken lin-41, including sites for the chicken orthologues of both C. elegans let-7 and lin-4. Finally, we show that these miRNAs and others are expressed in the chick limb consistent with the hypothesis that they regulate chicken Lin-41 activity in vivo.

Amino Acid Sequence↗
PubMed2005

miR-15a and miR-16-1 down-regulation in pituitary adenomas.

Micro RNAs (miRs) are small noncoding RNAs, functioning as antisense regulators of other RNAs. miR-15a and miR-16-1 genes are located at chromosome 13q14, a region which is frequently deleted in pituitary tumors. An inverse correlation has been shown in B cell chronic lymphocytic leukemia (B-CLL) between miR-15a and miR-16-1 expression and the expression levels of arginyl-tRNA synthetase (RARS), an enzyme which associates with the cofactor p43 in the aminoacyl-tRNA synthetase complex. When secreted, p43 regulates local inflammatory response and macrophage chemotaxis, and seems to have anti-neoplastic properties in mice. We explored miR-15a and miR-16-1 expression in 10 GH-secreting and in 10 PRL-secreting pituitary macroadenomas by Northern blot, and investigated the possible correlation with in vivo and in vitro characteristics. We found that miR-15a and miR-16-1 are expressed at lower levels in pituitary adenomas as compared to normal pituitary tissue. Moreover, their expression inversely correlates with tumor diameter and with RARS expression (P < 0.05), but directly correlates with p43 secretion (P < 0.02). Therefore, miR15 and miR16 down-regulation in pituitary adenomas correlates with a greater tumor diameter and a lower p43 secretion, suggesting that these genes may, at least in part, influence tumor growth.

Adenoma↗
PubMed2006

Expression profiles of micro RNA in proliferating and differentiating 32D murine myeloid cells.

32D cells are murine myeloid cells that grow indefinitely in Interleukin-3 (IL-3). In these cells, the type 1 insulin-like growth factor (IGF-I) and granulocytic-colony stimulating factor (G-CSF) induce differentiation to granulocytes. 32D cells do not express insulin receptor substrate-1 (IRS-1) or IRS-2, docking proteins of the IGF-I receptor. Ectopic expression of IRS-1 in these cells inhibits differentiation, the cells become IL-3 independent and IGF-1 dependent and can form tumors in mice. 32D and 32D-derived cells offer a good model in which to study the expression profiles of Micro Rna (miR) related to sustained proliferation or differentiation. We present here the data obtained with miR micro-arrays and identify the miR that are regulated by IGF-1 or G-CSF and are associated with either differentiation or indefinite cell proliferation of 32D murine myeloid cells.

Animals↗
PubMed2025

Balancing LncRNA H19 and miR-675 Bioconversion as a Key Regulator of Embryonic Myogenesis Under Maternal Obesity.

BACKGROUND: Maternal obesity (MO) impairs fetal skeletal muscle development, but the underlying mechanisms remain poorly defined. The regulatory roles of lncRNA H19 and its first exon derived microRNA675 (miR675) in prenatal muscle development remain to be examined. H19/Igf2 are in the same imprinting cluster with H19 expressed from the maternal allele while Igf2 expresses paternally. H19 contains a G-rich loop, and KH-type splicing regulatory protein (KHSRP) mediates the biogenesis of pre-miRNAs containing G-rich loops, which depends on its phosphorylation by AKT, a key mediator of IGF2 signalling. This study aims to depict the elusive function of these regulators that are affected by MO during embryonic myogenesis. METHODS: Single-cell transcriptomic sequencing and GeoMx spatial RNA sequencing were performed to identify the differentially expressed genes between embryos from MO and control (CT) mice. Both E11.5 and E13.5 embryos were collected and analysed to validate the sequencing data. The roles of H19 and miR657 in myogenesis were further analysed in P19 embryonic cells via CRISPR/dCas9-mediated H19 activation and inhibition. The epigenetic changes of H19 were analysed by methylated DNA immunoprecipitation, and allele-targeted analysis of H19 was performed by crossing C57BL/6J and CAST/EiJ mice. RESULTS: Transcriptomic analysis showed that MO embryos contained less differentiated myocytes (1.34%) than CT embryos (2.86%). Myogenesis-related GO biological processes were down-regulated in the MO embryonic myotome region. MO embryos showed lower expression of myogenic transcription factors such as Myf5, Myod1, Myog, Mef2c and Myh3 (p&#x2009;<&#x2009;0.05). MO altered epigenetic modifications of the H19 genomic cluster, showing a decreased methylation level in H19 imprinting control region (p&#x2009;<&#x2009;0.05) and a diallelic expression pattern of H19, which elevated its expression in MO embryos. Overexpression of H19 inhibited myogenesis in P19 cells, but miR675 promoted myogenesis, suggesting the critical regulatory roles of bioconversion of H19 to miR675. A KHSRP mediates the biogenesis of miR675, a process that relies on its phosphorylation by IGF2/AKT signalling. Knocking-down of KHSRP and inhibition of AKT abolished miR675 biogenesis. MO suppressed IGF2/AKT signalling and blocked KHSRP-dependent miR675 biogenesis in embryos. CONCLUSIONS: We found differential effects of H19 and miR675 on embryonic myogenesis. MO up-regulates H19 but blocks its miR675 bioconversion via suppressing IGF2/AKT/KHSRP signalling axis. Myogenesis in MO embryos was impeded due to the highly accumulated H19 and blocked miR675 biogenesis.

RNA, Long Noncoding↗
PubMed2006

Unusual gene order and organization of the sea urchin hox cluster.

While the highly consistent gene order and axial colinear patterns of expression seem to be a feature of vertebrate hox gene clusters, this pattern may be less well conserved across the rest of the bilaterians. We report the first deuterostome instance of an intact hox cluster with a unique gene order where the paralog groups are not expressed in a sequential manner. The finished sequence from BAC clones from the genome of the sea urchin, Strongylocentrotus purpuratus, reveals a gene order wherein the anterior genes (Hox1, Hox2 and Hox3) lie nearest the posterior genes in the cluster such that the most 3' gene is Hox5. (The gene order is 5'-Hox1, 2, 3, 11/13c, 11/13b, 11/13a, 9/10, 8, 7, 6, 5-3'.) The finished sequence result is corroborated by restriction mapping evidence and BAC-end scaffold analyses. Comparisons with a putative ancestral deuterostome Hox gene cluster suggest that the rearrangements leading to the sea urchin gene order were many and complex.

Animals↗
PubMed2004

Prevalence and distribution of HSV-1, VZV, and HHV-6 in human cranial nerve nuclei III, IV, VI, VII, and XII.

The etiology of idiopathic cranial nerve palsies often remains unresolved. It has been hypothesised that viral reactivation of herpesviruses in the corresponding nuclei in the brainstem is the cause. We investigated the distribution of herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) in nuclei that are associated with peripheral sensory ganglia [oculomotor (nIII), facial (nVII) nuclei] and in nuclei that are not associated with peripheral sensory ganglia [trochlear (nIV), abducens (nVI), and hypoglossal (nXII) nuclei] of five human brainstems. Samples of the cranial nerve nuclei and adjacent control tissue were taken from histological sections after precise identification of every single nucleus and control tissue. DNA and RNA amplification methods were used to determine the prevalence and distribution of HSV-1 and VZV. The distribution of human herpes virus type 6 (HHV-6) was also determined and served as a control, since HHV-6 infection has never been associated with idiopathic cranial nerve palsies. HSV-1 was distributed at random in all cranial nerve nuclei and control tissue, whereas VZV DNA was not detected in any of the samples examined. Surprisingly, HHV-6 was present in almost all samples where HSV-1 was also present, however, the latency associated transcript (LAT) of HSV-1 was not found in any of the samples positive for HSV-1 DNA. The absence of LAT in the samples positive for HSV-1 and the distribution of HSV-1 and HHV-6 do not support the hypothesis that idiopathic cranial nerve palsies result from viral reactivation in the brainstem nuclei.

Abducens Nerve↗
PubMed2025

KSHVbook: An Information-Sharing Database for Kaposi's Sarcoma-Associated Herpesvirus.

Kaposi's sarcoma-associated herpesvirus (KSHV) is a double-stranded DNA virus belonging to the &#x3b3;-herpesvirus subfamily. KSHV is the causative agent of Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), multicentric Castleman's disease (MCD), and KSHV inflammatory cytokine syndrome (KICS). Since its discovery, research on KSHV has rapidly progressed, but existing information platforms relatively lack comprehensiveness and do not provide efficient analysis tools tailored for KSHV. To further promote the research on KSHV more effectively, we have developed KSHVbook (http://www.kshvbook.com), a specialized information-sharing database dedicated to KSHV. This platform offers extensive information on genes, coding sequences, proteins, and the gene regulatory region. Besides, the KSHVbook includes about 35&#x2009;010 transcription factor binding sites (TFBSs), 342&#x2009;010 pairs of KSHV miRNA-host target gene relationships, protein structures predicted by AlphaFold3, qPCR primers, and so on. We also develop analytical tools for viral genome regions, TFBSs, and KSHV miRNA target genes to discover previously unknown biological functions of KSHV. These analytical tools can effectively identify the potential regulatory relationships between host transcription factors and viral genes. Overall, this platform provides a centralized data resource for KSHV research by integrating multiple databases, offering accessible analysis tools, and simplifying data acquisition. The KSHVbook will continue to be updated, and more features can be found on the website.

Herpesvirus 8, Human↗
PubMed2025

Dynamic Interplay Between miR-133a and RBMX During Dengue Virus Infection.

Viruses are obligate intracellular pathogens with limited genome capacity, relying entirely on host factors and cellular machinery for sustainable infection. In the present study, we demonstrate that dengue infection modulates the expression of RBMX (an RNA-binding protein) and miR-133a. Viral infection elevates the expression of the RBMX gene while downregulates the level of miR-133a. Additionally, Targetscan tool analysis shows that miR-133a possesses a potential binding site in the 3'UTR region of the RBMX gene, and our luciferase data indicate the miR-133a-mediated regulation of RBMX expression. Intriguingly, our time point study in Huh7 cells overexpressing the synthetic form of miR-133a mimic and inhibitor indicates the convoluted interaction between miR-133a and RBMX regulation during DENV infection. After 24&#x2009;h postinfection (hpi), miR-133a significantly suppresses both the RBMX expression and viral RNA levels, acting as an antiviral agent by targeting the expression of the RBMX gene. Additionally, our immunoprecipitation result suggested the central role of DENV 3'UTR in regulating the expression of both RBMX and miR-133a. Furthermore, our study on RBMX Overexpression illuminates the vital function of RBMX protein in the DENV life cycle. Overexpression of the RBMX gene in ivermectin-pretreated cells partially rescues viral replication. This comprehensive study explicates the dynamic miRNA/RBPs regulatory axis during DENV pathogenesis.

MicroRNAs↗
PubMed2026

Network based approach identifies miR-145-3p as a central regulatory hub associated to the progression from localized to metastatic medullary thyroid carcinoma.

Medullary thyroid carcinoma (MTC) is a neuroendocrine tumor originating from calcitonin producing C-cells and accounts for 1-5% of thyroid cancers. Total thyroidectomy is curative in localized disease (N0), whereas lymph node metastases (N1) are associated with poorer prognosis. However, the molecular mechanisms driving the metastatic shift remain poorly understood. This study aimed to identify miRNA features linked to metastatic spread in MTC, focusing on the transition from N0 to N1. Co-expression networks were constructed for N0 and N1 tumors, and differential connectivity analysis was used to identify key miRNAs acting as regulatory hubs. Functional annotation of their target genes was performed using the Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Ontology (GO), and Reactome pathway analyses. Validation experiments were carried out in MTC cells to evaluate the effects of selected miRNAs on cell proliferation, survival, and MAPK pathway activation. Network analysis revealed distinct miRNA co-expression patterns between N0 and N1 tumors. Differential network analysis highlighted miR-145-3p as a central regulatory hub, exhibiting 29 altered co-expression changes and a marked loss of connectivity in N1. Target enrichment identified 59 validated genes, including key oncogenic drivers such as MYC, PTEN, BCL2, PIK3CA, AKT1, and MAPK7. In MTC cells, simultaneous inhibition of miR-145-3p together with its top co-expressed miRNAs increased proliferation and survival, and enhanced ERK phosphorylation, indicating MAPK pathway activation and a shift toward a more aggressive phenotype. In conclusion, this study identifies a miRNA regulatory hub centered on miR-145-3p that is associated with metastatic progression and highlights the value of network-based approaches in uncovering mechanisms of cancer dissemination. &#xa9; 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

MAPK signaling↗
PubMed2002

Two genetic circuits repress the Caenorhabditis elegans heterochronic gene lin-28 after translation initiation.

The heterochronic gene lin-28 of the nematode Caenorhabditis elegans controls the relative timing of diverse developmental events during the animal's larval stages. lin-28 is stage-specifically regulated by two genetic circuits: negatively by the 22-nt RNA lin-4 and positively by the heterochronic gene lin-14. Here, we show that lin-28 is repressed during normal development by a mechanism that acts on its mRNA after translation initiation. We provide evidence that lin-14 inhibits a negative regulation that is independent of the lin-4 RNA and involves the gene daf-12, which encodes a nuclear hormone receptor. The lin-4-independent repression does not affect the initiation of translation on the lin-28 mRNA, and like the lin-4-mediated repression, acts through the gene's 3'-untranslated region. In addition, we find that lin-4 is not sufficient to cause repression of lin-28 if the lin-4-independent circuit is inhibited. Therefore, the lin-4-independent circuit likely contributes substantially to the down-regulation of lin-28 that occurs during normal development. The role of lin-4 may be to initiate or potentiate the lin-4-independent circuit. We speculate that a parallel lin-4-independent regulatory mechanism regulates the expression of lin-14.

Animals↗
PubMed2003

RNA silencing.

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Animals↗