RNASeq analysis to detect any molecular changes in skin of Dlx4 ablated mice compared to Wild type littermates.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE103971 | GEO | 2018/03/01
REPOSITORIES: GEO
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Project description:Homeobox proteins are known as master regulators of developmental morphogenesis. DLX genes encode transcription factors that significantly regulate the hematopoitic system. DLX4 and its isoform BP1 are expressed in different stages of development in human hematopoitic cells and regulate further differentiation. BP1 is the repressor of adult beta and delta globin genes found in fetal and embryonic tissues and rarely observed in adult tissues. In K562, a human chronic myelogenous leukemia cell line, BP1 is found to be over-expressed. In this study we have designed and synthesized a peptide-based artificial transcription factor that mimics the DNA binding domain of DLX4 homeodomain and can antagonise its binding. For the micro-array analysis we have taken peptide treated K562 cells and as control untreated K562 cells. Our study provides gene expression profile upon treatment of the homeodomain mimic.
2018-08-10 | GSE102390 | GEO
Project description:Homeobox genes encode transcription factors that control patterning of virtually all organ systems including the hematopoietic system. However, the role of homeobox genes in controlling development of the erythroid and megakaryocytic lineages is poorly understood. In this study, we investigated the role of the homeobox gene DLX4 in erythroid and megakaryocytic differentiation using the bipotent cell line K562 as a model. We compared the global gene expression profile of K562 cells that stably overexpressed DLX4 with that of vector-control K562 cells. As positive controls, global gene expression profiles were evaluated in vector-control K562 cells that were stimulated with Activin A (ActA) to induce erythroid differentiation and in vector-control K562 cells that were stimulated with phorbol 12-myristate 13-acetate (PMA) to induce megakaryocytic differentiation. Our study provides insights into the role of homeobox genes in controlling differentiation of the erythroid and megakaryocytic lineages. Three groups of samples were included: DLX4 vs Empty vector; Activin A vs None; PMA vs DMSO
2015-09-02 | E-GEOD-63888 | biostudies-arrayexpress
Project description:RNASeq analysis to detect any molecular changes in skin of Dlx4 ablated mice compared to Wild type littermates.
| PRJNA407807 | ENA
Project description:Homeobox genes encode transcription factors that control patterning of virtually all organ systems including the hematopoietic system. However, the role of homeobox genes in controlling development of the erythroid and megakaryocytic lineages is poorly understood. In this study, we investigated the role of the homeobox gene DLX4 in erythroid and megakaryocytic differentiation using the bipotent cell line K562 as a model. We compared the global gene expression profile of K562 cells that stably overexpressed DLX4 with that of vector-control K562 cells. As positive controls, global gene expression profiles were evaluated in vector-control K562 cells that were stimulated with Activin A (ActA) to induce erythroid differentiation and in vector-control K562 cells that were stimulated with phorbol 12-myristate 13-acetate (PMA) to induce megakaryocytic differentiation. Our study provides insights into the role of homeobox genes in controlling differentiation of the erythroid and megakaryocytic lineages.
2015-09-02 | GSE63888 | GEO
Project description:We report screening of genes differentially expressed in cells isolated from immature and mature third molar teeth. Among them, a homeobox transcription factor, distal-less homeobox 4 (DLX4) was highly expressed in immature human dental pulp cells, and significantly enhanced iPSC colony formation in combination with OCT3/4, SOX2, and KLF4 to the level comparable with that using classical combination of Yamanaka's factors, OCT3/4, SOX2, KLF4, and c-MYC.
2014-12-25 | GSE52853 | GEO
Project description:Background: The fibroblast-like synoviocyte (FLS) has a central role in rheumatoid arthritis (RA) pathogenesis and its invasive behavior strongly correlates with disease severity and joint damage. Yet, the regulation of FLS invasiveness is incompletely understood. Distal-less homeobox 4 (DLX4) is a transcription factor implicated in cancer cell invasion and metastasis, and we considered that it might also be involved in the regulation of FLS phenotypes. Results: siRNA knockdown of DLX4 significantly reduced RA FLS invasiveness (P=0.028) and migration in the scratch/wound healing assay (P=0.008). RNA sequencing analyses revealed that DLX4 knockdown significantly affected processes and pathways implicated in diverse types of cancer and in cancer biology and cell invasion, including cell cycle, DNA replication, transcription, p53 signal transduction, RHO GTPase signaling, regulation of cytokinesis, as well as response to oxygen levels and to oxidative stress. HMOX1 and SOD2 were among the genes with the most significantly increased expression, while CPNE3 and HADHA were among those with the most significantly decreased expression in FLS knocked down for DLX4 compared with controls. Conclusion: We describe a new role for DLX4 in the regulation of RA FLS behaviors relevant to disease pathogenesis and joint damage, and identify a new transcriptomic signature regulated by this gene. These findings raise the possibility that DLX4, or one of its target genes and pathways may become a target for treatment
2024-09-05 | GSE276473 | GEO
Project description:The Dlx homeobox genes have central roles in controlling patterning and differentiation of the brain and craniofacial primordia. In the brain, loss of Dlx function results in defects in the production, migration and differentiation of GABAergic neurons, that can lead to epilepsy. In the branchial arches, loss of Dlx function leads to craniofacial malformations that include trigeminal axon pathfinding defects. To determine how these genes function, we wish to identify the transcriptional circuitry that lies downstream of these transcription factors by comparing gene expression in wild type with Dlx mutant CNS and craniofacial tissues. 1) Compare gene expression in the maxillay branch of the first branchial arch (BA) of E10.5 wild type and Dlx2 -/- mutants. 2) Compare gene expression in the maxillary branch of the first BA of E10.5 wild type and Dlx1/2 -/- mutants. 3) Compare gene expression in wild type maxillary and mandibular branchial arches. 4) Compare gene expressionin mandibular branch of Dlx5/6 -/- mutants with wild type mandibular branch. The Dlx transcription factors are essential for controlling patterning of the brain and craniofacial primordia. In the brain, they control differentiation of GABAergic neurons of the basal ganglia. In the branchial arches, they control regional patterning. I hypothesize that there will be some conserved and some divergent mechanisms that the Dlx genes use in controlling brain and craniofacial development. We have already performed array analyses on Dlx function in the developing basal ganglia (with TGEN) by comparing expressed genes in wild type and Dlx1/2 mutants. Here we will compare gene expression in the brachial arches of wild type and Dlx mutant mice. 1) Generate E10.5 mouse embryos that are either wild type, Dlx2-/-, Dlx1/2 -/- or Dlx5/6 -/-. 2) Determine genotype by PCR. 3) Dissect branchial arches from the different genotypes. 4) Separate maxillary and mandibular branch of each branchial arch. 5) Prepare total RNA from the specimens. Obtain sufficient tissue to obtain 10 ug of total RNA - based on previous experience we anticipate that this will require ~ 10 branchial arches. We will pool the tissue from different embryos of the same genotype. 6) Send total RNA to TGEN for probe preparation, hybridization and array result analysis.
2008-06-13 | E-GEOD-4774 | biostudies-arrayexpress
Project description:DLX3 is a homeodomain transcription factor involved in ameloblast differentiation and enamel formation. Mutations in DLX3 in human lead to defects in enamel. However, the downstream targets of Dlx3 transcriptional activity in the enamel organ have not been identified yet. In this study, we compared the transcriptome of enamel organs where Dlx3 has been deleted to control tissues. Total RNA was extracted from enamel organs (mandibular incisors) from Dlx3-WT (N=4) and Dlx3-K14cKO (N=4) mice at P10. cDNA libraries were generated using NEBnext and NuGen kits. Sequencing was performed on the HiSeq2000.
2015-05-14 | E-GEOD-57984 | biostudies-arrayexpress
Project description:The Dlx homeobox genes have central roles in controlling patterning and differentiation of the brain and craniofacial primordia. In the brain, loss of Dlx function results in defects in the production, migration and differentiation of GABAergic neurons, that can lead to epilepsy. In the branchial arches, loss of Dlx function leads to craniofacial malformations that include trigeminal axon pathfinding defects. To determine how these genes function, we wish to identify the transcriptional circuitry that lies downstream of these transcription factors by comparing gene expression in wild type with Dlx mutant CNS and craniofacial tissues. 1) Compare gene expression in the maxillay branch of the first branchial arch (BA) of E10.5 wild type and Dlx2 -/- mutants. 2) Compare gene expression in the maxillary branch of the first BA of E10.5 wild type and Dlx1/2 -/- mutants. 3) Compare gene expression in wild type maxillary and mandibular branchial arches. 4) Compare gene expressionin mandibular branch of Dlx5/6 -/- mutants with wild type mandibular branch. The Dlx transcription factors are essential for controlling patterning of the brain and craniofacial primordia. In the brain, they control differentiation of GABAergic neurons of the basal ganglia. In the branchial arches, they control regional patterning. I hypothesize that there will be some conserved and some divergent mechanisms that the Dlx genes use in controlling brain and craniofacial development. We have already performed array analyses on Dlx function in the developing basal ganglia (with TGEN) by comparing expressed genes in wild type and Dlx1/2 mutants. Here we will compare gene expression in the brachial arches of wild type and Dlx mutant mice. 1) Generate E10.5 mouse embryos that are either wild type, Dlx2-/-, Dlx1/2 -/- or Dlx5/6 -/-. 2) Determine genotype by PCR. 3) Dissect branchial arches from the different genotypes. 4) Separate maxillary and mandibular branch of each branchial arch. 5) Prepare total RNA from the specimens. Obtain sufficient tissue to obtain 10 ug of total RNA - based on previous experience we anticipate that this will require ~ 10 branchial arches. We will pool the tissue from different embryos of the same genotype. 6) Send total RNA to TGEN for probe preparation, hybridization and array result analysis. Keywords: other
2006-06-06 | GSE4774 | GEO
Project description:Dlx3 over-expression in mouse embryonic fibroblasts changed the expression level of numerous genes involved in osteogenesis and embryonic stem cell-related pathways as revealed by microarray analysis. From the list of Dlx3 modulated genes we focused our attention on the study of two candidates, Lifr and Chrdl1. Chromatin immunoprecipitation demonstrated the recruitment of Dlx3 transcription factor to the promoters of Lifr and Chrdl1, and luciferase assays confirmed the role of Dlx3 in the regulation of Lifr expression. Over-expression of Dlx3 in mouse embryonic stem cells stimulated Lifr and Chrdl1 expression and inhibited expression of Id proteins and Bmp4. We show that Dlx3 increases the expression of both soluble and transmembrane forms of Lifr. Soluble Lifr may regulate extracellular Lif levels via solution binding, while transmembrane Lifr mediates the signal transduction pathway. The data suggests that Dlx3 may be involved in stem cell differentiation in a dosage dependent way through its interaction with Lifr and with Chrdl1, a known antagonist of Bmp4. We speculate that Dlx3 may also be involved in osteoblast differentiation through interactions involving Lifr, Bmp, and Id proteins and signaling via the JAK/STAT and MAPK pathways. In summary, our data suggests that Dlx3 proteins play a significant role in a highly tuned network in early embryogenesis. Keywords: treated vs.untreated Stable and Transient transfection of Dlx3 in MEF. Total of 4 hybridizations including biological replicates.
2009-08-15 | E-GEOD-11727 | biostudies-arrayexpress