Examplepictures of DNA-Structures
Monday Tuesday Wednesday Thursday Friday Saturday Sunday
44
31
1
2
3
45
4
7
10
46
12
16
17
47
19
20
21
22
23
24
48
26
27
30
1

Seite 2 von 2 12 <<

November 01 - November 30

14 Einträge gefunden

CRTD (RAC B..
Startdatum: November 18
04:00 pm 06:00 pm

Beschreibung: 

Program

4:00 - 4:30:        Yannick Fuchs, Bonifacio Lab, CRTD
                           "Single cell RNAseq based Immune cell characterization in Type 1 diabetes"

4:30 - 5:00:        Theresia Gutmann, Coskun Lab, PLID
                           "CryoEM structure of the ligand-saturated insulin receptor ectodomain"

5:00 - 5:30:        Mohamed Elgendy, Institute for Clinical Chemistry and Laboratory Medicine and Medical Clinic I, UKD
                           "Intermittent Fasting with Metformin for Targeting Tumor Metabolism: Two Are Better Than One."

5:30 - 6:00:        Discussion and social get-together

 
Host:    Dr. Ünal Coskun (On behalf of Triantafyllos Chavakis)

Date:    Monday, 18th November 2019

Time:    4:00 pm - 6:00 pm

Place:   CRTD, auditorium left


Join the discussion afterwards, incl. drinks and snacks.

Everybody is very welcome!

Aged Relate..
Startdatum: November 25
05:00 pm 06:00 pm

Beschreibung: 

Abstract:

Humans are exceptionally long-lived in comparison to other primates, with a projected maximum lifespan of ~115 years. This extreme longevity presents unique challenges to many of the post-mitotic cells that compose our bodies and makes us highly susceptible to age-associated diseases (AADs) such as cancer, diabetes, and various neurodegenerative diseases.  In the first part of this presentation I will address the key features of aging that appear to drive neurodegeneration, compare the iPSC and direct conversion approaches for next-generation human cellular modeling, and discuss the extent to which iNs reflect aged neurons.

Human neurons contain high levels of somatic genomic variations that might derive from DNA double-strand break (DSB) intermediates. For the second part of my presentation, we applied high throughput genome-wide translocation sequencing to study replication stress-induced DSB hotspots, and identified replication-associated genomic fragile regions overlapping genes in neural progenitor cells (NPCs) derived from human pluripotent stem cells. Our results demonstrate that replication-associated genome instability may lead to neurological dysfunction by disrupting long neural genes linked to neurodevelopmental diseases.

Genetic mec..
Startdatum: November 28
04:00 pm 05:00 pm

Beschreibung: 

Abstract:
"Most genetic mechanisms that are currently known to underlie developmental processes and human diseases have been discovered by analyzing a very small fraction of the genome that encodes for protein-coding sequences. Recent studies have revealed that large portions of the noncoding genome contain functional regulatory elements and noncoding transcripts. It is thus reasonable to presume that understanding the function of such elements can shed new light into developmental and cellular mechanisms, and uncover new causes of human disease.

Recent work has shown that common DNA variants in human pancreatic islet enhancers contribute to the risk of developing common polygenic forms of type 2 diabetes. Many of these diabetes risk variants are located in islet enhancer hubs that typically control multiple cell-specific target genes. The current challenge lies in using this information to dissect the mechanisms through which these regulatory variants impact pancreatic islets and polygenic diabetes. This effort could be assisted by the analysis of rare highly penetrant natural or artificial mutations, which can be used to provide insights into how noncoding DNA variants contribute to disease mechanisms.

Rare recessive mutations in an enhancer near PTF1A have been shown to cause neonatal diabetes associated with severe pancreas hypoplasia. I will discuss how modeling mutations in this enhancer provide unsuspected insights into the developmental and molecular mechanisms that underpin this regulatory defect.

Defects in long noncoding RNAs (lncRNAs) provide another potential mechanism of disease. Inhibition of several lncRNAs can impact gene expression and insulin secretion in cellular assays, but their physiological and disease relevance remains largely unexplored. I will discuss a genetic model that shows how disruption of a lncRNA can lead to severe pancreatic beta cell dysfunction and diabetes."

Publications:

* Human pancreatic islet 3D chromatin architecture provides insights into the genetics
of type 2 diabetes
Irene Miguel-Escalada, Silvia Bonàs-Guarch, Inês Cebola, Joan Ponsa-Cobas, Julen Mendieta-Esteban, Delphine M.Y. Rolando, Biola M. Javierre, Goutham Atla, Irene Farabella, Claire C. Morgan, Javier García-Hurtado, Anthony Beucher, Ignasi Morán, Lorenzo Pasquali, Mireia Ramos, Emil V.R. Appel, Allan Linneberg, Anette P. Gjesing, Daniel R. Witte, Oluf Pedersen, Niels Garup, Philippe Ravassard, David Torrents, Josep Maria Mercader, Lorenzo Piemonti, Thierry Berney, Eelco J.P. de Koning, Julie Kerr-Conte, François Pattou, Iryna O. Fedko, Inga Prokopenko, Torben Hansen, Marc A. Marti-Renom, Peter Fraser, Ferrer J
Biorxiv doi: https://doi.org/10.1101/400291.
 
* Human pancreatic β cell lncRNAs control cell-specific regulatory networks.
Akerman I, Tu Z, Beucher A, Rolando D, Sauty-Colace C, Benazra M, Nakic N, Yang J, Wang H, Pasquali L, Moran I, Garcia-Hurtado J, Castro N, Gonzalez-Franco R, Stewart A, Bonner C, Piemonti L, Berney T, Groop L, Kerr-Conte J, Pattou F, Argmann C, Schadt E, Ravassard P, Ferrer J.
Cell Metab. 2017 February 7;25, 1–12. doi: 10.1016/j.cmet.2016.11.016.
 
* Pasquali L*, Gaulton KJ*, Rodriques-Segul SA*, Mularoni L, Miguel-Escalada I, Akerman I, Tena JJ, Moran I, Gomez-Marin C, van de Bunt M, Ponsa-Cobas J, Castro N, Nammo T, Cebola I, Garcia-Hurtado J, Maestro MA, Pattou F, Piemonti L, Berney T, Gloyn AL, Ravassard P, Gomez-Skarmeta JL, Mueller F, McCarthy MI, Ferrer J. Pancreatic islet enhancer cluster enriched in type 2 diabetes risk-associated
variants.
Nature Genetics 2014 Feb 46 (2): 136-43, * Equal contribution
 
* Pancreatic exocrine duct cells give rise to insulin-producing ß-cells during
embryogenesis but not after birth.
Solar M*, Cardalda C*, Houbracken I*, Martín M, Maestro M, De Medts N, Xu X, Grau V, Heimberg H, Bouwens L, Ferrer J.
Dev Cell, 2009 Dec; 17 ( 6): 849-860. *equal contribution PMID: 20059954

“A sweet vi..
Startdatum: November 29
04:00 pm 05:00 pm

Beschreibung: 

Abstract “A sweet view on biomaterials engineering”:

The molecular recognition of glycosaminoglycans (GAGs) such as hyaluronan (HA) and chondroitin sulfate (CS) by a variety of proteins in the extracellular matrix (ECM) is crucial for physiological processes such as tissue hemostasis and repair, cell growth and cell-migration. Therefore, chemically modified GAG derivatives constitute relevant molecules for the engineering of innovative biomaterials with application in tissue regeneration. We investigate the molecular recognition properties of several defined sulfated oligohyaluronan (sHA) and CS derivatives toward a set of regulatory proteins of the extracellular matrix (i.e. interleukin 8 (IL-8), sclerostin and vascular endothelial growth factor (VEGF)) using computational approaches (i.e. docking, molecular dynamics and binding free energy calculations) in combination with experimental techniques (i.e. fluorescence polarization, surface plasmon resonance and isothermal titration calorimetry) [1-6]. We will present a selection of these studies showing how defined GAGs chemical substitutions affect binding to the target protein in terms of strength, site and mode [5-6]. We use the obtained information to rationally design GAGs with customized properties for the engineering of new biomaterials for skin and bone regeneration.

Abstract “Single-cell immune profiling in health and disease”:

Type I diabetes (T1D) is a chronic organ-specific disease, which is characterized by a deficiency in endogenous insulin production, and it arises as the result of autoreactive immune cell-mediated destruction of insulin-producing beta-cells in the pancreas. Beta-cell targeted autoimmunity is already underway before the appearance of symptoms, and it is thought to be triggered by a combination of genetic and environmental factors, giving rise to autoreactive cells. Autoreactive T cells are considered the main effectors of beta-cell destruction, and CD8+ T cells are the predominant T cell population and most abundant inflammatory cell type in insulitis. The main antigen recognition tool of T cells is T cell receptor (TCR) expressed on their plasma membrane. However, other immune cell types are also present in the pancreatic infiltrate and can contribute either directly (CD4+ T cells, NK cells, B cells) or indirectly (macrophages, dendritic cells) to beta-cell death. Using 10xGenomics, a single-cell RNA sequencing (scRNA-Seq) platform that allows for simultaneous epitope and transcriptome measurement, and reconstruction of TCRs/BCRs in a paired manner, I would to like identify memory CD8+ T cell TCRs and memory B cell BCRs that confer specificity for different antigens and T1D relevant antigen peptides in patients at risk or at onset of T1D. Using samples from early childhood, this knowledge can then be used to potentially pinpoint the initiating event(s) causing autoimmunity and help to understand underlying autoimmune mechanisms that lead to T1D development.

 

... followed by Social Hour!

Seite 2 von 2 12 <<

To the top of this page.