Expression data from 22 human myotubes (7 healthy controls, 4 Dysferlinopathy (DYSF), 4 Caveolinopathy 3 (CAV3), 4 Facioscapulohumeral muscular dystrophy(FSHD) and 3 Four and a half LIM 1 protein deficiency FHL1).cDNA microarray data showed that cyclin A1 levels are specifically elevated in FSHD vs. other muscular disorders such as CAV3, DYSF, FHL1 and healthy control. Data could be confirmed with RT-PCR and Western blot analysis showing up-regulated levels of cyclin A1 also on the protein level.
Altered expression of cyclin A 1 in muscle of patients with facioscapulohumeral muscle dystrophy (FSHD-1).
Age, Specimen part, Disease, Disease stage
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Melanoma-associated cancer-testis antigen 16 (CT16) regulates the expression of apoptotic and antiapoptotic genes and promotes cell survival.
Cell line, Treatment
View SamplesThe cellular gene expression profiles were investigated in CT16 (PAGE5) negative WM-266-4 melanoma cells as well as in the WM-266-4 cells expressing transfected CT16 cDNA.
Melanoma-associated cancer-testis antigen 16 (CT16) regulates the expression of apoptotic and antiapoptotic genes and promotes cell survival.
Cell line
View SamplesIn the normal prostate, most basal and some luminal cells are castration-resistant (CR). The identity of these CR cells and their relation to CR prostate cancer are unresolved. We compared single-cell expression profiles of prostate cells sorted from hormonally nave (HN) and castrated mice. We found both basal and luminal-localized cells, particularly the latter, were molecularly heterogeneous. CR luminal cells and a subset of HN luminal cells exhibited a similar intermediate expression pattern, including high-level expression of multiple prostate stem/progenitor marker genes and androgen receptor gene. We validated LY6D as a marker linking CR luminal cells to luminal progenitors. LY6D+ prostate cells, including LY6D+ luminal cells, were enriched for organoid-forming potential regardless of the presence or absence of androgen. Krt8-based lineage-tracing revealed that LY6D+ CR luminal cells produced LY6D- normal luminal cells upon regeneration, but LY6D+ luminal cancer cells under PTEN-deficiency. Furthermore, prostate cancers originating from CR luminal cells (LY6D+) exhibited a more advanced phenotype than those from HN luminal cells (LY6D+ or LY6D-). Lastly, LY6D amplification/upregulation appear associated with advanced prostate cancer in patient samples. Together, our studies demonstrate LY6D as a novel progenitor marker predictive of lethal CR disease.
Single-Cell Analysis Identifies LY6D as a Marker Linking Castration-Resistant Prostate Luminal Cells to Prostate Progenitors and Cancer.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Epigenetic regulator Smchd1 functions as a tumor suppressor.
Specimen part
View SamplesSmchd1 appears to act as a tumour suppressor in the transformed fibroblast model. We find gene expression differences are most pronounced in the transformed MEFs. We always detect a small number of clustered genes and imprinted genes as differentially expressed, along with others involved in tumorigenesis.
Epigenetic regulator Smchd1 functions as a tumor suppressor.
Specimen part
View SamplesSmchd1 appears to act as a tumour suppressor in the E-Myc B cell lymphoma model. We find gene expression differences are most pronounced in the premalignant cells, and observe more variability in end stage lymphomas. We always detect a small number of clustered genes and imprinted genes as differentially expressed, along with others involved in tumorigenesis.
Epigenetic regulator Smchd1 functions as a tumor suppressor.
Specimen part
View SamplesSmchd1 appears to act as a tumour suppressor in the E-Myc B cell lymphoma model. We find gene expression differences are most pronounced in premalignant cells. We always detect a small number of clustered genes and imprinted genes as differentially expressed, along with others involved in tumorigenesis.
Epigenetic regulator Smchd1 functions as a tumor suppressor.
Specimen part
View SamplesSmchd1 appears to act as a tumour suppressor in the E-Myc mouse B cell lymphoma model. We find a small number of gene expression differences at E17.5 in the pre-B cells, before phenotypic differences are observed.
Epigenetic regulator Smchd1 functions as a tumor suppressor.
Specimen part
View SamplesWe report the deregulation of expression in E9.5 male mouse embryos are that homozygous for a mutant allele of the Smchd1 gene (ie Smchd1MommeD1/MommeD1). Overall design: RNA-seq analysis of Smchd1+/+ vs Smchd1MommeD1/MommeD1
Smchd1 regulates a subset of autosomal genes subject to monoallelic expression in addition to being critical for X inactivation.
Sex, Subject
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