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accession-icon GSE140662
Expression data of keratinocytes from condyloma acuminata and skin tissues
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

To explore the biological changes of keratinocytes in condyloma acuminata (CA) warts, we performed mRNA and lncRNA expression profiling of keratinocytes from normal skins and warts of condyloma acuminata patients to compare the gene expression.

Publication Title

Enhanced Glycogen Metabolism Supports the Survival and Proliferation of HPV-Infected Keratinocytes in Condylomata Acuminata.

Sample Metadata Fields

Specimen part

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accession-icon GSE86870
Genome-wide transcriptional analysis of metabolism-related genes and pathways regulated by FAH in melanoma A375 cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Reprogramming metabolism plays an important role in tumor cells for maintaining their abnormal biologic behaviors. Therefore, special factors could regulate metabolic processes and influence the overall status of tumor cells. This phenomenon was obviously found in melanoma. Fumarylacetoacetate hydrolase (fumarylacetoacetase, FAH) is an enzyme encoded by the FAH gene located on the chromosome 15q25.1 region and contains 14 exons. FAH enzyme catalyzes the hydrolysis of 4- fumarylacetoacetase into fumarate and acetoacetate. It is the last enzyme in the subpathway from L-phenylalanine and tyrosine degradation. Mutations in the FAH gene cause type I tyrosinemia, which is a hereditary error of metabolism that is characterized by increased tyrosine levels in the blood and urine of patients. In the present study, we will explore whether FAH is an essential enzyme to promote multiple metabolic processes and elucidate the functions of FAH in melanoma. Gene microarrays and bioinformatics analysis of the differentially expressed genes (DEGs) were performed using A375 cells, and we concentrated on the biologic functions of FAH. In general, our work revealed several functional mechanisms of FAH in melanoma, which indicated FAH might be a potentially therapeutic target and an independent prognostic indicator for this disease.

Publication Title

CDC5L drives FAH expression to promote metabolic reprogramming in melanoma.

Sample Metadata Fields

Cell line

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accession-icon GSE73613
Expression data from normal breast tissues and invasive primary breast carcinoma tissues
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The role of lymphangiogenesis in tumor metastasis remains unclear. This study addressed this issue in lymphatic endothelial cells (LECs) derived from primary invasive breast cancer specimens.

Publication Title

Tumor-associated Lymphatic Endothelial Cells Promote Lymphatic Metastasis By Highly Expressing and Secreting SEMA4C.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE93695
Antidyskinetic effects of MEK inhibitor are associated with multiple neurochemical alterations in the striatum of hemiparkinsonian rats
  • organism-icon Rattus norvegicus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.0 ST Array (ragene20st)

Description

L-DOPA-induced dyskinesia (LID) represents one of the major problems of the long-term therapy of patients with Parkinson's disease (PD). Although the pathophysiologic mechanisms underlying LID are not completely understood, activation of the extracellular signal regulated kinase (ERK) is recognized to play a key role. ERK is phosphorylated by mitogen-activated protein kinase kinase (MEK), and thus MEK inhibitor can prevent ERK activation. Here the effect of the MEK inhibitor PD98059 on LID and the associated molecular changes were examined. Rats with unilateral 6-OHDA lesions of the nigrostriatal pathway received daily L-DOPA treatment for three weeks, and abnormal involuntary movements (AIMs) were assessed every other day. PD98059 was injected in the lateral ventricle daily for 12 days starting from day 10 of L-DOPA treatment. Striatal molecular markers of LID were analyzed together with gene regulation using microarray. The administration of PD98059 significantly reduced AIMs. In addition, ERK activation and other associated molecular changes including FosB were reversed in rats treated with the MEK inhibitor. PD98059 induced significant up-regulation of 418 transcripts and down-regulation of 378 transcripts in the striatum. Tyrosine hydroxylase (Th) and aryl hydrocarbon receptor nuclear translocator (Arnt) genes were down-regulated in lesioned animals and up-regulated in L-DOPA-treated animals. Analysis of protein levels showed that PD98059 reduced the striatal TH. These results support the association of p-ERK1/2, FosB, p-H3 to the regulation of TH and ARNT in the mechanisms of LID, and pinpoint other gene regulatory changes, thus providing clues for identifying new targets for LID therapy.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage

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accession-icon GSE105763
MBD2 Ablation Impairs Lymphopoiesis and Impedes Progression and Maintenance of T-cell Acute Lymphoblastic Leukemia
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Little is known about the roles of methyl-CpG-binding domain protein 2 (MBD2), a reader of DNA methylation, in T-cell acute lymphoblastic leukemia (T-ALL). Here, we investigated the role of MBD2 in T-ALL by using an Mbd2 knockout mouse model. We found that MBD2 ablation impeded the progression and maintenance of Notch1-driven T-ALL.Our data reveals essential roles for MBD2 in lymphopoiesis and T-ALL and support an intriguing potential of MBD2 as a therapeutic target for T-ALL.

Publication Title

MBD2 Ablation Impairs Lymphopoiesis and Impedes Progression and Maintenance of T-ALL.

Sample Metadata Fields

Specimen part

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accession-icon GSE87850
Expression data of siFAM210B and control A549 cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Our previous study screened a novel cancer progression suppressor gene, FAM210B, which encodes an outer mitochondrial membrane protein, by the suppression of mortality by antisense rescue technique (SMART). We demonstrated that FAM210B loss was significantly associated with cancer metastasis and decreased survival in a clinical setting.

Publication Title

No associated publication

Sample Metadata Fields

Cell line

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accession-icon GSE97172
Targets of Bmi1 in HCC pathogenesis
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE97170
Gene expression in the liver of Bmi1 knockout mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To explore the potential targets of Bmi1 in the liver development of hepatic carcinogenesis, we assayed the gene expression level in the liver of Bmi1 knockout mice. We isolated the liver tissue of Bmi1 WT and KO mice around 6-8 weeks. Then we extracted total RNA and run the microarray detection. Gene expression in Bmi1 KO mouse livers was compared with that in Bmi1 WT mouse livers to screen potential targets of Bmi1.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE97169
Gene expression in the Bmi1 knockout Huh7 and Hep3B cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Bmi1 plays a pivotal role in hepatic carcinoma (HCC), but its targets in HCC is unknown. To screen the potential targets, we transfected HCC cell line Huh7 and Hep3B with Bmi1 shRNA lenti-virus. After confirming the Bmi1 was knocked down using western blotting, we extracted total RNA and then run the microarray detection. Gene expression profiles in Bmi1 KO cells were compared with those in Bmi1 WT cells to screen potential targets of Bmi1.

Publication Title

No associated publication

Sample Metadata Fields

Cell line

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accession-icon GSE20493
Transcriptional profiling of an Fd-GOGAT1/GLU1 mutant in Arabidopsis thaliana
  • organism-icon Arabidopsis thaliana
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Transcriptional profiling of an Fd-GOGAT1/GLU1 mutant in Arabidopsis thaliana reveals a multiple stress response and extensive reprogramming of the transcriptome

Publication Title

Transcriptional profiling of an Fd-GOGAT1/GLU1 mutant in Arabidopsis thaliana reveals a multiple stress response and extensive reprogramming of the transcriptome.

Sample Metadata Fields

Specimen part

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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