Marcel Schulz

74 Followers
35 Following
279 Posts
Computational Biology, Group Leader @goetheuni Frankfurt
Group websitehttps://schulzlab.github.io
GitHub accounthttps://github.com/SchulzLab

RT @SFB1531
📢 We are very much looking forward to the next Joint Research Meeting Heart | Kidney | Vessel on May, 26!

Don't miss these three exciting talks!

#JRMHeartKidneyVessel @TheMarcelSchulz @DimmelerLab @BrandesLab @m_leistner @IVS_FFM

RT @itisalist
You have ChIP/ATAC- and RNA-seq data and want to learn more about essential transcription factors? Check out our tool TF-prioritizer which was just published in @GigaScience with @MarkusHoffmann2 @nico_trummer @TheMarcelSchulz @cosybio_UHH @dbblumenthal https://doi.org/10.1093/gigascience/giad026

RT @sinabooeshaghi
I am excited to share another preprint with @lpachter and Fan Gao. We explain a method (called snATAK) for preprocessing single nuclei ATAC seq data.

https://www.biorxiv.org/content/10.1101/2021.12.08.471788v2

RT @heinig_matthias
1/7 How do genetic variants affect co-expression patterns and how can this help us to interpret consequences of GWAS hits? In our latest preprint, we use scRNAseq to find such associations by mapping co-expression QTLs (co-eQTL)! https://doi.org/10.1186/s13059-023-02897-x
Identification of genetic variants that impact gene co-expression relationships using large-scale single-cell data - Genome Biology

Background Expression quantitative trait loci (eQTL) studies show how genetic variants affect downstream gene expression. Single-cell data allows reconstruction of personalized co-expression networks and therefore the identification of SNPs altering co-expression patterns (co-expression QTLs, co-eQTLs) and the affected upstream regulatory processes using a limited number of individuals. Results We conduct a co-eQTL meta-analysis across four scRNA-seq peripheral blood mononuclear cell datasets using a novel filtering strategy followed by a permutation-based multiple testing approach. Before the analysis, we evaluate the co-expression patterns required for co-eQTL identification using different external resources. We identify a robust set of cell-type-specific co-eQTLs for 72 independent SNPs affecting 946 gene pairs. These co-eQTLs are replicated in a large bulk cohort and provide novel insights into how disease-associated variants alter regulatory networks. One co-eQTL SNP, rs1131017, that is associated with several autoimmune diseases, affects the co-expression of RPS26 with other ribosomal genes. Interestingly, specifically in T cells, the SNP additionally affects co-expression of RPS26 and a group of genes associated with T cell activation and autoimmune disease. Among these genes, we identify enrichment for targets of five T-cell-activation-related transcription factors whose binding sites harbor rs1131017. This reveals a previously overlooked process and pinpoints potential regulators that could explain the association of rs1131017 with autoimmune diseases. Conclusion Our co-eQTL results highlight the importance of studying context-specific gene regulation to understand the biological implications of genetic variation. With the expected growth of sc-eQTL datasets, our strategy and technical guidelines will facilitate future co-eQTL identification, further elucidating unknown disease mechanisms.

BioMed Central

RT @tomaspueyo
Starship is about to change the world, but ppl haven't realized yet

@SpaceX and @elonmusk's rocket will drop transportation costs to space

And in the past, every drop in transportation costs has revolutionized the world.

Here's what's going to happen:

RT @hillermich
Happy to share our TOGA manuscript, now out in Science. Project started 6 years ago, we and others already used TOGA in numerous projects. TOGA integrates gene annotation and orthology inference, and scales to hundreds of genomes. https://www.science.org/doi/10.1126/science.abn3107
RT @AlexBickMDPhD
Clonal hematopoiesis of indeterminate potential no longer ... out in @NEJMEvidence today @Lachelle_Dawn presents a clinically useful risk score to prognosticate risk of malignant transformation & death in patients with #CHIP & #CCUS https://evidence.nejm.org/doi/full/10.1056/EVIDoa2200310
http://www.chrsapp.com
RT @ImranSHaque
Tweetorial time! We @RecursionPharma mapped consequences of #CRISPR screening of >17K human genes, found a systematic bias confounding all CRISPR screens, traced its molecular cause, and propose a debiasing algorithm.

RT @minouye271
The strongest polygenic risk scores I've seen are for autoimmune diseases, e.g. type 1 diabetes and ankylosing spongylitis (cuz HLA of course)

Anyone seen another disease with PRS AUC~0.92-93 (or even better)?

T1D paper https://diabetesjournals.org/care/article/42/2/200/30342/Development-and-Standardization-of-an-Improved

AS paper https://ard.bmj.com/content/80/9/1168.long

Development and Standardization of an Improved Type 1 Diabetes Genetic Risk Score for Use in Newborn Screening and Incident Diagnosis

OBJECTIVE. Previously generated genetic risk scores (GRSs) for type 1 diabetes (T1D) have not captured all known information at non-HLA loci or, particularly, a

American Diabetes Association

RT @MuenchLab
📣We profiled host cell responses after infection with different #SARSCoV2 variants. Omicron showed a strikingly delayed immune response!

https://doi.org/10.1016/j.mcpro.2023.100537

Great teamwork by @TharyanGeorge and Melinda from @CiesekSandra lab et al.

@IBC2_GU,@dfg_public,@EnableFrankfurt