To identify transcription factors critically involved in the Tfh cell transcriptional network, antigen-specific Tfh and non-Tfh cells from a day 8 immune response were analyzed by RNA-seq. Overall design: Ovalbumin-specific T cells from OT-II TCR-transgenic mice were transferred into C57BL/6 recipients, which were immunized subcutaneously with nitrophenol coupled to ovalbumin. Eight days after immunization, transgenic T cells from pooled inguinal lymph nodes were sorted for a CD44hi CXCR5+ PD-1+ Tfh and CD44hi CXCR5- PD-1- non-Tfh cell phenotype for analysis by RNA-seq.
Bach2 Controls T Follicular Helper Cells by Direct Repression of Bcl-6.
Specimen part, SubjectView Samples
Polarity defects are a hallmark of most carcinomas. Cells from invasive micropapillary carcinomas (IMPCs) of the breast are characterized by a striking cell polarity inversion and represent a good model for the analysis of polarity abnormalities. We have performed an in-depth investigation of polarity alterations in 24 IMPCs, compared with invasive carcinomas of no special type (ICNST).
LIN7A is a major determinant of cell-polarity defects in breast carcinomas.
Specimen partView Samples
3 pairs of wt and ClC-6 knockout mice, RNA from p14 hippocampus
Lysosomal storage disease upon disruption of the neuronal chloride transport protein ClC-6.
Sex, Age, Specimen part, Subject, TimeView Samples
The maintenance of the TFH phenotype depends on continuous signals via ICOS. For a global assessment of differences in gene expression after interruption of the ICOS pathway a genome wide transcriptome analysis was performed. We used the OT-II adoptive transfer system to isolate antigen-specific TFH cells (day 6 after immunization) after short-term (6 hours) blockade of the ICOS pathway using a monoclonal antibody against ICOS-L.
ICOS maintains the T follicular helper cell phenotype by down-regulating Krüppel-like factor 2.
Sex, Specimen part, TreatmentView Samples
Microarray used to detail the global gene transcription underlying sorted IFNg+ and IFNg- Tregs (CD4+CD25+CD127lo) and Tconv (CD4+CD25-CD127+) for fresh (unexpanded) and 14 day expanded cells from human blood.
Divergent Phenotypes of Human Regulatory T Cells Expressing the Receptors TIGIT and CD226.
Specimen part, Disease stage, Treatment, SubjectView Samples
Gene expression was compared between medullary breast carcinoma (MBC) and non medullary basal-like breast carcinoma (non-MBC BLC).
Medullary Breast Carcinoma, a Triple-Negative Breast Cancer Associated with BCLG Overexpression.
Disease, Disease stageView Samples
IPF (n=20) and control (n=19) samples were obtained through the LTRC and were sequenced on an Illumina HiSeq 2000 following TruSeq RNA Sample Prep Kit v2 library preparation. Overall design: Cross-sectional samples were analyzed. IPF diagnosis was based on American Thoracic Society and European Respiratory Society criteria, and all IPF samples displayed typical patterns of usual interstitial pneumonia. RNA libraries were prepared from 200 ng of high quality total RNA according to the manufacturer’s instructions for the TruSeq RNA Sample Prep Kit v2 (Illumina, San Diego, CA). The concentration and size distribution of TruSeq libraries was determined on an Agilent Bioanalyzer DNA 1000 chip (Santa Clara, CA), and a final quantification, using Qubit fluorometry (Invitrogen, Carlsbad, CA), was conducted to confirm sample concentration. Libraries were loaded onto paired end flow cells at concentrations of 8-10 pM to generate cluster densities of 700,000/mm2 following Illumina’s standard protocol using the Illumina cBot and cBot Paired end cluster kit version 3. The flow cells were sequenced as 51 X 2 paired end reads on an Illumina HiSeq 2000 using TruSeq SBS sequencing kit version 3 and SCS version 1.4.8 data collection software. Base-calling was performed using Illumina’s RTA version 188.8.131.52.
Cellular senescence mediates fibrotic pulmonary disease.
Specimen part, Disease, Disease stage, SubjectView Samples
Although protein acetylation is widely observed, it has been associated with few specific regulatory functions making it poorly understood. To interrogate its functionality, we analyzed the acetylome in Escherichia coli knockout mutants of cobB, the only known sirtuin-like deacetylase, and patZ, the best-known protein acetyltransferase. For four growth conditions, more than 2,000 unique acetylated peptides, belonging to 809 proteins, were identified and differentially quantified. Nearly 65% of these proteins are related to metabolism. The global activity of CobB contributes to the deacetylation of a large number of substrates and has a major impact on physiology. Apart from the regulation of acetyl-CoA synthetase, we found that CobB-controlled acetylation of isocitrate lyase contributes to the fine-tuning of the glyoxylate shunt. Acetylation of the transcription factor RcsB prevents DNA binding, activating flagella biosynthesis and motility, and increases acid stress susceptibility. Surprisingly, deletion of patZ increased acetylation in acetate cultures, which suggests that it regulates the levels of acetylating agents. The results presented offer new insights into functional roles of protein acetylation in metabolic fitness and global cell regulation.
Protein acetylation affects acetate metabolism, motility and acid stress response in Escherichia coli.
No sample metadata fieldsView Samples
Alzheimer's disease is a devastating neurodegenerative disease eventually leading to dementia. An effective treatment does not yet exist. Here we show that oral application of the compound anle138b restores hippocampal synaptic and transcriptional plasticity as well as spatial memory in a mouse model for Alzheimer's disease, when given orally before or after the onset of pathology. At the mechanistic level we provide evidence that anle138b blocks the formation of conducting Aß pores without changing the membrane embedded Aß-oligomer structure. In conclusion, our data suggest that anle138b is a novel and promising compound to treat AD-related pathology that should be investigated further. Overall design: APPdelta9 and Wildtype mouse treated with anle138b or placebo
The diphenylpyrazole compound anle138b blocks Aβ channels and rescues disease phenotypes in a mouse model for amyloid pathology.
Age, Cell line, SubjectView Samples