scholarly journals Identification of a specific gene expression pattern associated with HCV-induced pathogenesis in HCV- and HCV/HIV-infected individuals

Virology ◽  
2006 ◽  
Vol 350 (2) ◽  
pp. 453-464 ◽  
Author(s):  
Kathie-Anne Walters ◽  
Maria W. Smith ◽  
Sampa Pal ◽  
Jill C. Thompson ◽  
Matthew J. Thomas ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Pattern ◽  
Gene Expression Pattern ◽  
Specific Gene ◽  
Specific Gene Expression

scholarly journals Drosophila Sister-of-Sex-lethal reinforces a male-specific gene expression pattern by controlling Sex-lethal alternative splicing

2018 ◽  
Vol 47 (5) ◽  
pp. 2276-2288 ◽  
Author(s):  
Rebecca Moschall ◽  
Mathias Rass ◽  
Oliver Rossbach ◽  
Gerhard Lehmann ◽  
Lars Kullmann ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alternative Splicing ◽  
Expression Pattern ◽  
Gene Expression Pattern ◽  
Specific Gene ◽  
Specific Gene Expression ◽  
Sex Lethal ◽  
Male Specific

scholarly journals Repression precedes independent evolutionary gains of a highly specific gene expression pattern

Cell Reports ◽  
2021 ◽  
Vol 37 (4) ◽  
pp. 109896
Author(s):  
Jian Pu ◽  
Zinan Wang ◽  
Haosu Cong ◽  
Jacqueline S.R. Chin ◽  
Jessa Justen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Pattern ◽  
Gene Expression Pattern ◽  
Specific Gene ◽  
Specific Gene Expression

Cdx1 or Cdx2 expression activates E-cadherin-mediated cell-cell adhesion and compaction in human COLO 205 cells

2004 ◽  
Vol 287 (1) ◽  
pp. G104-G114 ◽  
Author(s):  
Matthew S. Keller ◽  
Toshihiko Ezaki ◽  
Rong-Jun Guo ◽  
John P. Lynch
Keyword(s):  
Gene Expression ◽  
Cell Adhesion ◽  
Gene Expression Pattern ◽  
Cell Junctions ◽  
Specific Gene ◽  
Specific Response ◽  
Specific Gene Expression ◽  
Cdx2 Expression ◽  
E Cadherin ◽  
Cell Cell

A mature columnar intestinal epithelium develops late in embryogenesis and is maintained throughout the life of the organism. Although the mechanisms driving intestine-specific gene expression have been well studied, those promoting the acquisition of cell-cell junctions, columnar morphogenesis, and polarization have been less studied. The Cdx homeodomain transcription factors (Cdx1 and Cdx2) regulate intestine-specific gene expression and intestinal epithelial differentiation. We report here that Cdx expression induces E-cadherin activity and cell-cell adhesion in human COLO 205 cancer cells. Within days of Cdx1 or Cdx2 expression, a new homotypic cell-cell adhesion phenotype is induced. This is a specific response to Cdx, inasmuch as a Cdx1 mutant failed to elicit the effect. Additionally, Cdx-expressing COLO 205 cells demonstrate a reduced proliferative capacity and an increase in the mRNA expression of differentiation-associated genes. Electron micrographs of these cells demonstrate induction of tight, adherens, and desmosomal junctions, as well as a columnar shape and apical microvilli. Investigations of the adhesion phenotype determined that it was Ca2+dependent and could be blocked by an E-cadherin-blocking antibody. However, E-cadherin protein levels and intracellular distribution were unchanged. Cdx expression restored the ability of the cell membranes to adhere and undergo compaction. We conclude that Cdx1 or Cdx2 expression is sufficient to induce an E-cadherin-dependent adhesion of COLO 205 cells. This adhesion is associated with polarization and cell-cell membrane compaction, as well as induction of a differentiated gene-expression pattern. Ascertaining the mechanism for this novel Cdx effect may yield insight into the development of mature colonic epithelium.

scholarly journals Intronic enhancers regulate the expression of genes involved in tissue-specific functions and homeostasis

2020 ◽  
Author(s):  
Beatrice Borsari ◽  
Pablo Villegas-Mirón ◽  
Hafid Laayouni ◽  
Alba Segarra-Casas ◽  
Jaume Bertranpetit ◽  
...  
Keyword(s):  
Gene Expression ◽  
Embryonic Stem ◽  
Gene Expression Pattern ◽  
Specific Gene ◽  
Control Of Gene Expression ◽  
Tissue Specific ◽  
Tissue Specific Gene ◽  
Specific Gene Expression ◽  
Expression Of Genes ◽  
Genomic Location

AbstractTissue function and homeostasis reflect the gene expression signature by which the combination of ubiquitous and tissue-specific genes contribute to the tissue maintenance and stimuli-responsive function. Enhancers are central to control this tissue-specific gene expression pattern. Here, we explore the correlation between the genomic location of enhancers and their role in tissue-specific gene expression. We found that enhancers showing tissue-specific activity are highly enriched in intronic regions and regulate the expression of genes involved in tissue-specific functions, while housekeeping genes are more often controlled by intergenic enhancers. Notably, an intergenic-to-intronic active enhancers continuum is observed in the transition from developmental to adult stages: the most differentiated tissues present higher rates of intronic enhancers, while the lowest rates are observed in embryonic stem cells. Altogether, our results suggest that the genomic location of active enhancers is key for the tissue-specific control of gene expression.

High Rate of FLT3 Mutations In Adult ETP-ALL.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1031-1031 ◽  
Author(s):  
Martin Neumann ◽  
Ebru Coskun ◽  
Ouidad Benlasfer ◽  
Sandra Heesch ◽  
Stefan Schwartz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cell ◽  
Expression Pattern ◽  
Mirna Expression ◽  
Lymphoblastic Leukemia ◽  
Specific Gene ◽  
Wild Type ◽  
Specific Gene Expression ◽  
Flt3 Mutation ◽  
Flt3 Mutations

Abstract Abstract 1031 Introduction: Mutations of FLT3 are recognized as important prognostic factor in acute myeloid leukemia (AML) with an impact on new therapeutic strategies. However, FLT3 mutations are rarely (1-3%) found in acute T-lymphoblastic leukemia (T-ALL). Recently, a new T-ALL subgroup defined by a specific gene expression profile and a characteristic immunophenotype (CD1a-, CD8-, CD5weak with expression of stem cell or myeloid markers) and with poor outcome has been described in pediatric T-ALL patients. This subgroup likely originates from early thymic progenitors (ETP) and has therefore been termed ETP-ALL. To unravel the molecular alterations of this distinct subgroup with myeloid characteristics, we studied adult ETP-ALL patients for FLT3 mutations. Moreover, we analyzed miRNA expression to explore their potential involvement in the specific gene expression signature observed in ETP-ALL. Patients and methods: We screened 1241 peripheral blood and bone marrow samples of T-ALL patients that were sent to the central diagnostic reference laboratory of the German Acute Lymphoblastic Leukemia Multicenter Study Group (GMALL). Of the immunophenotypically identified ETP-ALL patients (n=142), sufficient material was available in 70 cases. FLT3 mutations (ITD and TKD) were assessed using the FLT3 mutation assay (InVivoScribe Technologies, San Diego, USA). Expression of miRNAs was first screened by TaqMan low density arrays including 667 miRNAs in ETP-ALL (n=8) and compared to non-ETP T-ALL (n=6). Subsequently, expression of miR-221 and miR-222 was examined by real-time PCR in all 70 ETP-ALL. Results: In our cohort of 1241 T-ALL, 142 (11.4 %) patients showed an immunophenotype of an ETP-ALL, which is in the range of reported frequencies in pediatric patients. Among the 70 ETP-ALL samples analyzed, we identified 9 patients with a FLT3 D835 mutation and 15 patients with a FLT3 ITD. In total, 34 % (24 of the 70) patients carried a FLT3 mutation, which represents approximately 4 % of all T-ALL patients. In contrast, only one patient was identified with a FLT3 mutation within an arbitrarily selected control group of 107 T-ALL patients with a non-ETP immunophenotype. Interestingly, ETP-ALL with FLT3 mutations showed a distinct immunophentype compared to ETP-ALL with a wild type FLT3: ETP-ALL with FLT3 mutations had a higher rate of positivity for CD2 (88% vs. 30%, P<0.001), CD117 (83% vs. 28%, P<0.001), and CD13 (100 % vs. 37%, P<0.001). On the other hand, ETP-ALL with wild type FLT3 were characterized by a more frequent positivity of CD5 (54% vs. 4%, P<0.001) and CD33 (54% vs. 4%, P<0.001). Based on these findings a specific immunophenotype may be linked to FLT3 mutated ETP-ALL: in 73% (21/29) of patients with CD2/CD13 positivity a FLT3 mutation was present, compared to only 7% (3/41) of the remaining patients with ETP-ALL. In addition, we generated miRNA expression profiles in ETP-ALL and identified 7 miRNAs that were differentially expressed compared to non-ETP T-ALL. Among these miR-221 and miR-222, which were significantly overexpressed in ETP-ALL, are targeting genes characterizing the ETP-ALL phenotype (e.g. ETS1, KIT). Examination of miR-221 and miR-222 in 70 ETP-ALL revealed their particular overexpression in FLT3 mutated samples (miR-221 2.45-fold, P=0.012; miR-222: 2.05-fold, P=0.008) compared to ETP-ALL with wild type FLT3. Conclusion: We identified a yet unreported high frequency of FLT3 mutations in T-ALL, which are nearly exclusively found within the subgroup of ETP-ALL. In this group the rate is comparable high to the rate of FLT3 mutations in AML. Therefore, on the basis of established flow cytometry analysis we identified T-ALL patients that should be now prospectively and routinely screened for FLT3 mutations. Moreover, the distinct miRNA expression pattern may impact on the specific gene expression pattern of ETP-ALL. Thus, patients of this molecular distinct ETP-ALL entity may benefit from tyrosine kinase inhibitors in relapse situations or with presence of minimal residual disease as a bridging therapy to allogeneic stem cell transplantation. Disclosures: Baldus: Novartis: Research Funding.

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