• microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. (cancerindex.org)
  • Circular RNAs (circRNAs), a novel type of non-coding RNAs (ncRNAs), are ubiquitously expressed in eukaryotic cells during post-transcriptional processes. (ijbs.com)
  • ncRNAs play important roles in controlling gene expression at both transcriptional and post-transcriptional levels. (ijbs.com)
  • They are important post-transcriptional regulators of gene expression in plants, metazoans, and mammals, and are predicted to control the activity of 30% of all protein-coding genes [ 2 ]. (biomedcentral.com)
  • In this review, we focus on the impact of ncRNA post-transcriptional regulatory mechanisms, especially those of microRNAs and lncRNAs, in RA signalling pathways during differentiation and disease. (mdpi.com)
  • HIV-1-infected podocytes showed markedly elevated cyclin D 1 mRNA and cyclin D 1 protein, the latter of which did not down-regulate during cell-cell contact or differentiation, suggesting post-transcriptional stabilization of cyclin D 1 protein levels by HIV-1. (biomedcentral.com)
  • 1) For example, the down-regulation of miR15s and miR - 16 - 1 in chronic lymphocytic leukaemia, prostate cancer and pituitary tumours, leading to the inhibition of tumour growth and induce cell cycle arrest at the G 1 - phase by target cell cycle regulators ( cyclin D1, cyclin E1, cyclin D3 and CDK6). (ukessays.com)
  • Furthermore people of different sign transduction pathways regulate cyclin D appearance favorably (e.g. the changing mutant p21ras and p42/p44MAPK) or adversely (e.g. p38) (1 2 28 40 Nevertheless the transcriptional systems that hyperlink mitogenic sign transduction to cyclin D appearance are poorly understood. (bibf1120.com)
  • This cyclin forms a complex with and functions as a regulatory subunit of CDK4 or CDK6, whose activity is required for cell cycle G1/S transition. (ayassbioscience.com)
  • It has been shown to form complex with Hsp90 and a variety of protein kinases including CDK4, CDK6, SRC, RAF-1, MOK, as well as eIF2 alpha kinases. (nih.gov)
  • Amplification of the Sonic Hedgehog pathway is the best characterized subgroup, with 25% of human tumors having mutations in Patched, Sufu (Suppressor of Fused Homolog), Smoothened, or other genes in this pathway. (wikipedia.org)
  • Further, we review the corresponding genes and the proteins encoded by these genes, their possible role in the developing brain and reported mutations of these genes. (biomedcentral.com)
  • DUSP4 alterations lead to hyperactivation of MAPK signaling in many cancers, including breast cancer, which often harbor mutations in cell cycle checkpoint genes, particularly in TP53. (biomedcentral.com)
  • Comparative transcriptomic analysis of tumor cells from diseased mice revealed the expression of several well-known MLL-rearranged leukemia-associated target genes, including Meis1 , Runx1 ( pMIRH-128a mice), HoxA9 , Flt3 ( pMIRH-130b mice), Cdk6 , and Bcl2 . (ashpublications.org)
  • Phosphorylation of EIF2S1/eIF2α is an important mechanism that can regulate all three UPR pathways through transcriptional and translational reprogramming to maintain cellular homeostasis and overcome cellular stresses. (bvsalud.org)
  • Actionable mutations enriched in homologous recombination repair, cell cycle, and phosphoinositide 3-kinase/AKT/mammalian target of rapamycin pathways were detected in 60% of HGESS patients. (e-crt.org)
  • Together, these results illustrate the co regulation of EGF receptors, their downstream signaling pathways, and their transcriptional targets. (hdac-inhibitors.com)
  • A plausible mechanism for how signaling from these pathways is integrated into a transcriptional response is offered by the remaining module, six. (hdac-inhibitors.com)
  • Transcriptional integration of upstream signaling Examination of M6 unveiled an enrichment for TFs together with other nuclear proteins involved in cell cycle regulation, chromatin modifications, and epigenetic regulation. (hdac-inhibitors.com)
  • On top of that, JUN, MYC, and RELA signify mem bers of every from the transcription factor households recognized inside the enhancer examination, which we implicate in our chromatin mediated transcriptional suggestions hypothesis. (hdac-inhibitors.com)
  • It is predicted that MCPH gene mutations may lead to the disease phenotype due to a disturbed mitotic spindle orientation, premature chromosomal condensation, signalling response as a result of damaged DNA, microtubule dynamics, transcriptional control or a few other hidden centrosomal mechanisms that can regulate the number of neurons produced by neuronal precursor cells. (biomedcentral.com)
  • Dr. Gray has also developed structure-based, generalized approaches for designing drugs to overcome one of the most common mechanisms of resistance observed against most kinase inhibitor drugs, mutation of the so-called 'gatekeeper' residue, which has been observed in resistance to drugs targeting BCR-ABL, c-KIT and PDGFR. (stanford.edu)
  • BLBCs are nearly always accompanied by inactivating mutations in TP53 , encoding p53 [ 15 ]. (biomedcentral.com)
  • TP53 and DNMT3A mutations were the most frequent mutations. (e-crt.org)
  • Studies have therefore proposed that blocking ACVR1 kinase activity may represent a useful therapeutic strategy for the DIPG subgroup carrying ACVR1 mutations 14 , 17 . (nature.com)
  • JOA displayed the activity of inhibiting the BCR-ABL and promoted differentiation of not only imatinib -sensitive but also imatinib -resistant cells with BCR-ABL mutation, which could become a potent lead compound to overcome the imatinib -resistant induced by inhibitors of BCR-ABL tyrosine kinase in CML therapy. (jcancer.org)
  • Icotinib is a potent and highly selective oral epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), and it is used for the first-line treatment of locally advanced or metastatic non-small cell lung cancer (NSCLC) patients carrying EGFR mutations. (bettapharma.com)
  • Recently, we reported that the nucleus-mitochondria positive feedback loop formed by p90 ribosomal S6 kinase (p90RSK) and phosphorylation of S496 on ERK5 (a unique member of the mitogen-activated protein kinase family that is not only a kinase but also a transcriptional co-activator) were vital signaling events that played crucial roles in linking mitochondrial dysfunction, nuclear telomere dysfunction, persistent SASP induction, and atherosclerosis. (oaepublish.com)
  • Mutations, amplification and overexpression of this gene, which alters cell cycle progression, are observed frequently in a variety of human cancers. (ayassbioscience.com)
  • For instance, overexpression of cyclins or the elimination of CDK inhibitors or pRB due to genetic mutation are common cause in human cancer. (ukessays.com)
  • We find that together with loss-of-function mutations in p53 and, to some degree, potentiated by cMyc overexpression, Dusp4 deletion aids in cell cycle checkpoint escape while simultaneously potentiating hallmarks of replicative stress, including multinucleation and Chk1 phosphorylation. (biomedcentral.com)
  • Also, a subgroup-specific alternative splicing further confirms the existence of distinct subgroups and highlights the transcriptional heterogeneity between subgroups. (wikipedia.org)
  • Mutations in this gene as well as in its related proteins including D-type cyclins, p16(INK4a) and Rb were all found to be associated with tumorigenesis of a variety of cancers. (thermofisher.com)
  • 1 MLL-AF4 binding upstream of the miR-128a and miR-130b transcriptional start sites suggested direct regulation. (ashpublications.org)
  • The most frequent mutation in DIPG is a lysine to methionine (K27M) mutation that occurs on H3F3A or HIST1H3B/C , encoding histone variants H3.3 and H3.1 (refs. (nature.com)
  • Gain-of-function mutations in the oncogenes KRAS and BRAF are also frequent findings in early stages of transformation [ 6 ]. (biomedcentral.com)
  • Scope includes mutations and abnormal protein expression. (cancerindex.org)
  • Although ACVR1 mutations have been implicated in the pathogenesis of this currently incurable disease, the impacts of bone morphogenetic protein (BMP) signaling on more than 60% of H3K27M DIPG carrying ACVR1 wild-type remain unknown. (nature.com)
  • Recruits and targets histone methyltransferases SUV39H1, KMT5B and KMT5C, leading to epigenetic transcriptional repression. (abcam.cn)
  • A mutation in this gene resulting in reduced cell proliferation, and impaired cell motility and polarity, and has been identified in patients with primary microcephaly. (cancerindex.org)
  • MCPH is inherited in an autosomal recessive pattern in which both copies of the gene in each cell have mutations. (biomedcentral.com)
  • Single-cell RNA-sequencing (scRNA-seq) analysis of thousands of DIPG tumor cells containing H3K27M mutations showed that most of these tumor cells resemble oligodendrocyte precursor cells (OPC-like)-a cell type that exhibits obviously enhanced proliferation and tumor-propagating potential compared with other cell subsets in tumor samples 9 . (nature.com)
  • Here, we determined the effect of Jiyuan oridonin A (JOA), an ent -kaurene diterpenoid compound, on the differentiation blockade in imatinib-sensitive, particularly, imatinib-resistant CML cells with BCR-ABL-T315I mutation by cell proliferation assay, apoptosis analysis, cell differentiation analysis, cell cycle analysis and colony formation assay. (jcancer.org)
  • We found that JOA at lower concentration significantly inhibited the proliferation of CML cells expressing mutant BCR-ABL (T315I mutation included) and wild-type BCR-ABL, which was due to that JOA induced the cell differentiation and the cell cycle arrest at G0/G1 phase. (jcancer.org)
  • This study identifies a novel mechanism for breast tumorigenesis implicating Dusp4 loss and p53 mutations in cellular acquisition of Dbf4 upregulation as a driver of cellular replication and cell cycle checkpoint escape. (biomedcentral.com)
  • The Influence of Pathological Mutations and Proline Substitutions in TDP-43 Glycine-Rich Peptides on Its Amyloid Properties and Cellular Toxicity. (bio-rad-antibodies.com)
  • Hence, it seems reasonable that research and potential therapeutic strategies for these two subtypes of DIPG should be tailored specifically, focused on the now-known differential impacts of the H3.1K27M versus H3.3K27M mutations on cancer epigenomes. (nature.com)
  • The HAND2 transcriptional regulator controls cardiac development, and we uncover additional essential functions in the endothelial to mesenchymal transition (EMT) underlying cardiac cushion development in the atrioventricular canal (AVC). (devgenbasel.com)
  • The research attention given to the role of BMP signaling in DIPG has so far strongly emphasized the ACVR1 mutation DIPG subtype. (nature.com)
  • Amplification of the Sonic Hedgehog pathway is the best characterized subgroup, with 25% of human tumors having mutations in Patched, Sufu (Suppressor of Fused Homolog), Smoothened, or other genes in this pathway. (wikipedia.org)
  • CLL leukemic cells are either derived from a naive B lymphocyte without somatic hypermutation of the immunoglobulin heavy-chain variable region gene ( IgVH ) mutation, or a post-germinal center B cell with somatic IgVH mutation. (medscape.com)
  • The molecular pathogenesis of liver cancer (i.e., hepatocellular carcinoma [HCC]) is a multistep process that involves both genetic changes, such as chromosomal abnormalities and mutations of the DNA sequence (i.e., somatic mutations), and epigenetic mechanisms, such as chemical modifications of the DNA and the histone proteins around which the DNA is wrapped to form the chromosomes, microRNA posttranscriptional regulators, and changes in various signaling pathways (Wong et al. (nih.gov)
  • The catenin beta 1 gene (CTNNB1) encodes the β-catenin protein, and mutations in CTNNB1 occur widely in HB. (biomedcentral.com)
  • Mutations in CTNNB1 are closely related to HB and are most likely the original aberrations leading to tumorigenesis. (biomedcentral.com)
  • [ 80 ] Interestingly, CLL patients with IgVH gene mutation fare better with higher complete response rate, progression-free and overall survival (OS), than those without IgVH gene mutation. (medscape.com)
  • Cells may begin to transform in an early stage of liver differentiation, or the transformation may be caused by gene mutation after liver development completed. (biomedcentral.com)
  • Genomic characterization reveals distinct mutation landscapes and therapeutic implications in neuroendocrine carcinomas of the gastrointestinal tract. (cdc.gov)
  • The landscape of genomic mutations in cancer reveals that many mutations or copy number changes in cancer are frequently located in noncoding DNA regions [ 1 , 4 ]. (biomedcentral.com)
  • Oncogenic mutations in these cells can cause cancers that maintain a hierarchical organization reminiscent of the tissue of origin. (nature.com)
  • Epigenetic regulation is an umbrella term that encompasses several mechanisms such as DNA methylation, histone post-translational modifications (PTMs), nucleosome remodeling, histone variants, and RNA-mediated post-transcriptional regulation. (encyclopedia.pub)
  • reduced class in dimerization chains Phosphodiesterase 3B( PDE3B) which is subsequent interaction( mutations)( targeted in Manning and Toker 2017). (evakoch.com)
  • Our approach enables the identification of LSC-specific gene expression programs and the characterization of differentiation blocks induced by leukemic mutations. (nature.com)
  • In 10-20% of healthy individuals over age 70, the acquisition of pre-leukemic mutations in hematopoietic stem cells (HSCs) results in the dominance of a small number of HSC-derived clones, a process termed Clonal Hematopoiesis of Indeterminate Potential (CHIP) 6 , 7 . (nature.com)
  • As a result, in CLLs with del(11q) (leading to loss of miR-34b/c ) or del(17p) (resulting in failure of transcriptional activation of miR-34a and miR-34b/c ) would lead to lack of translational repression of the ZAP70 gene, and hence associated with high ZAP70 protein expression and a poor prognosis. (medscape.com)
  • The package enables flexible programmatic access to CellMiner's unparalleled breadth of NCI-60 data, including gene and protein expression, copy number, whole exome mutations, as well as activity data for ∼21K compounds, with information on their structure, mechanism of action and repeat screens. (nih.gov)
  • Also, a subgroup-specific alternative splicing further confirms the existence of distinct subgroups and highlights the transcriptional heterogeneity between subgroups. (wikipedia.org)
  • It can regulate gene expression at the post transcriptional level by binding to the 3′ untranslated region (UTR) of target mRNAs, Which leads to cleavage of the target mRNA by the Ago2 ribonuclease in the RNA induced silencing complex (RISC) or inhibition of translation [ 6 ]. (jcancer.org)
  • We generated stable SELENBP1-overexpression and their corresponding control cell lines to determine its potential effect on cell cycle and transcriptional activity of p21 by using flow cytometry and luciferase reporter assay, respectively. (biomedcentral.com)
  • Also substrate for SMAD3, phosphorylating SMAD3 in a cell-cycle-dependent manner and repressing its transcriptional activity. (nih.gov)
  • Exhibits transcriptional corepressor activity with INSM1 on the NEUROD1 and INS promoters in a cell cycle-independent manner. (nih.gov)
  • p27 regulated the cell cycle and inhibited cell proliferation by affecting formation of the cell cycle-dependent complex CDK6/CCND1, but did not directly affect the expression of CDK6 and CCND1. (omicsdi.org)
  • Post-transcriptional suppression of EZH2 expression not only blocked STAT3 mediated miR-21 trans-activation, but also reversed the miR-200a/b silencing via reducing DNMT1 and H3K27me3 expressions. (jcancer.org)
  • ihc_assay_report ihc assay report C173071 CTDC Node Terminology C99752 Indel Mutation A mutation class that includes insertion mutations, deletion mutations and mutation events where both an insertion and a deletion has occurred. (nih.gov)
  • copy_number_variant copy number variant C173071 CTDC Node Terminology C171175 Delins Mutation A change in a nucleotide sequence where nucleotides in a reference sequence are replaced by other nucleotides and which is not a substitution, inversion or conversion. (nih.gov)