This SuperSeries is composed of the SubSeries listed below.
Human but not mouse adipogenesis is critically dependent on LMO3.
Specimen part, Treatment
View SamplesWe aimed at identifying lymphangiogenic subpopulations by comparative analysis of single cell clones derived from a melanoma of a single patient. Selected clones were grafted into SCID mice, where they induced lymphangiogenesis and metastasized into sentinel nodes, whereas non-lymphangiogenic clones from the same patient did not metastasize. RNA isolated from primary SCID mouse tumors were used for transcriptome analysis.
MET expression in melanoma correlates with a lymphangiogenic phenotype.
No sample metadata fields
View SamplesMyeloid cells can inhibit the anti-tumor responses of T cells. The mechanism for this cross-talk is not fully elucidated but is known to require STAT3.
No associated publication
Specimen part, Disease, Disease stage
View SamplesAutophagy is a mechanism that regulates cellular metabolism and clearance of damaged macromolecules and organelles. Impaired degradation of modified macromolecules contributes to cellular dysfunction and is observed in aged tissue and senescent cells. We have inactivated Atg7, an essential autophagy gene, in murine keratinocytes and have found in an earlier study that this resulted in increased baseline oxidative stress and reduced capacity to degrade crosslinked proteins after oxidative ultraviolet stress. To investigate whether autophagy deficiency would promote cellular aging, we studied, how Atg7 deficient (KO) and Atg7 bearing cells (WT) would respond to stress induced by Paraquat (PQ), an oxidant drug commonly used to induce cellular senescence.
Autophagy deficient keratinocytes display increased DNA damage, senescence and aberrant lipid composition after oxidative stress in vitro and in vivo.
No sample metadata fields
View SamplesIn this study we aimed to gain further insight on the role of GCs in adipocyte differentiation. For the future drugability of candidate targets it is of utmost importance to find factors relevant to human biology. Thus, we analyzed the transcriptome of GC induced primary human adipose stem cells (hASC) to identify novel factors downstream of GC action
Human but not mouse adipogenesis is critically dependent on LMO3.
Specimen part
View SamplesCord blood stem cells were expanded and differentiated to NK cells. Samples taken at different days after induction of differentiation were analyzed and compared to undifferentiated expanded stem cells. The most highly upregulated genes were further analyzed.
The Transcription Factor ZNF683/HOBIT Regulates Human NK-Cell Development.
Specimen part, Time
View SamplesAngiogenesis, the formation of new capillaries by sprouting from preexisting vessels, is mainly induced by VEGF-A. To identify genes which are induced by VEGF-A in endothelial cells and genes which are differently expressed or VEGF-A induced in HUVEC and CEP, HUVEC and CEP were starved and induced by VEGF-A165 for 30, 60 and 150min. RNA of induced and uninduced cells was isolated and subjected to microarray analysis using Affymetrix microarray.
No associated publication
Specimen part, Treatment, Time
View SamplesHLX was found as a VEGF-A induced gene in HUVEC (B.Schweighofer, submitted). In order to detect genes regulated by HLX HUVEC were infected by recombinant adenovirus expressing HLX for 4, 8, 16 and 32h. RNA was isolated and subjected to microarray analysis using Affymetrix microarray.
The VEGF-regulated transcription factor HLX controls the expression of guidance cues and negatively regulates sprouting of endothelial cells.
No sample metadata fields
View SamplesNCoR1 (Nuclear receptor Co-Repressor) and SMRT (Silencing Mediator of Retinoid and Thyroid hormone receptor) are well-recognized coregulators of nuclear receptor (NR) action. However, their unique roles in the regulation of thyroid hormone (TH) signaling in specific cell types have not been determined. To accomplish this we generated a mouse model that lacked function of either NCoR1 or SMRT or both in the liver only. Despite both corepressors being present in the liver, SMRT had no ability to regulate TH signaling when deleted in either euthyroid or hypothyroid animals. In contrast, disruption of NCoR1 action confirmed that it is the principal mediator of TH sensitivity in vivo. While SMRT played little role in TH signaling alone, when disrupted in combination with NCoR1 it greatly accentuated the activation of hepatic lipogenesis regulated by NCoR1. Thus, corepressor specificity exists in vivo and NCoR1 is the principal regulator of TH action in the liver. However, both NCoR1 and SMRT collaborate to control hepatic lipogenesis and lipid storage, which likely reflects their cooperative activity in regulating the action of multiple NRs including the thyroid hormone receptor (TR).
NCoR1 and SMRT play unique roles in thyroid hormone action in vivo.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
HO-1 inhibits preadipocyte proliferation and differentiation at the onset of obesity via ROS dependent activation of Akt2.
Specimen part
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