Research

Invited speaker: Natalia Soshnikova

We have the pleasure of hosting Dr. Natalia Soshnikova from the Institute of Molecular Biology gGmbH (IMB) in Mainz, Germany. She will talk about the molecular mechanisms of intestinal stem cell specification during development.

More details about her research here: Soshnikova Lab

Date: Thursday 18th of January
Time: 10:30 – 11:10 + discussions
Place: BUS1: Meeting-room Pankreas (6th floor, KGJ for Diabetes)

Microsoft Word - SEMINAR-Natalia.docx
Some Selected Papers produced by the Soshnikova lab:

  • Dzama MM, Nigmatullina L, Sayols S, Kreim N and Soshnikova N (2017). Distinct populations of embryonic epithelial progenitors generate Lgr5+ intestinal stem cells. Dev Biol, pii: S0012-1606(17)30576-6. doi: 10.1016/j.ydbio.2017.10.012
  • Kazakevych J, Sayols S, Messner B, Krienke C and Soshnikova N (2017). Dynamic changes in chromatin states accompany specification of the adult intestinal stem cells. Nucleic Acids Res, 45(10):5770-5784. doi: 10.1093/nar/gkx167
  • Nigmatullina L, Norkin M, Dzama MM, Messner B, Sayols S, Soshnikova N (2017). Id2 controls specification of Lgr5+ intestinal stem cell progenitors during gut development. EMBO J, 36: 869-885. doi: 10.15252/embj.201694959 (recommended by F1000Prime)
  • Jung H, Mazzoni EO, Soshnikova N, Hanley O, Venkatesh B, Duboule D, Dasen JS (2014). Evolving Hox activity profiles govern diversity in locomotor systems. Dev Cell, 29, 171-187
  • Schorderet P, Lonfat N, Darbellay F, Tschopp P, Gitto S, Soshnikova N, Duboule D (2013). A genetic approach to the recruitment of PRC2 at the HoxD locus. PLoS Genet, 9, e1003951
  • Montavon T, Soshnikova N, Mascrez B, Joye E, Thevenet L, Splinter E, de Laat W, Spitz F and Duboule D (2011). A regulatory archipelago controls Hox genes transcription in digits. Cell, 147, 1132-1145
  • Soshnikova N, Montavon T, Leleu M, Galjart N and Duboule D (2010). Functional analysis of CTCF during mammalian limb development. Dev Cell, 19, 819-830
  • Soshnikova N and Duboule D (2009). Epigenetic temporal control of mouse Hox genes in vivo. Science, 324, 1320-1323

Please share with your colleagues and students, and show your support by attending the seminar.

 

 

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BSCC Christmas seminar: Anne Mette Søviknes

We would like to invite you to the BSCC Christmas seminar on Friday, December 15th, 12:00 o’clock at Birkhaugsalen. For details, please see the attached poster. 

Please share with your colleagues and students, and show your support by attending the seminar.

 

2017-12-15 BSCC Christmas seminar 2017

Stamcelleforskning – i dag og i morgen

Program for stamcelleforskning (2013–2017) har hatt som mål å utvikle og styrke kompetansen innenfor grunnleggende og klinisk forskning på stamceller, med sikte på behandling av alvorlig og kronisk syke pasienter.

Programmet har hatt tre hovedpilarer: Støtte til prosjekter basert på åpen konkurransebasert utlysning av forsknings- midler, bevilgning til Nasjonalt senter for stamcelleforskning, og finansiering av det årlige nettverksmøtet for norsk stamcelleforskning. Programstyret har gjennom disse virkemidlene bygget opp norsk stamcelleforskning.

Programmet har hatt fire prioriterte tematiske områder:
• Forskning for bedre forståelse av basale prosesser knyttet til vekst og differensiering av stamceller.
• Karakterisering og validering av stamceller for bruk i klinikken.
• Utvikling og implementering av prosedyrer og protokoller for reparasjon av skadet vev eller organ.
• Bruk og videreutvikling av induserte pluripotente stamceller (iPS-celler).

Mer informasjon på programmets hjemmeside.

Formidlingsbrosjyre Program for stamcelleforskning

 

 

Norwegian Press Reviews

We are very grateful and happy to announce that our research article was discussed in several interviews, where Helge explained the current status of diabetes research and our contribution. You can find the the press articles (in Norwegian) below:

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interview for nrk

interview for forskning.no

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Screen Shot 2017-08-16 at 14.32.28

 

 

New Article: Scientific Reports

Maturity-onset diabetes of the young (MODY) is one of the hereditary forms of diabetes mellitus caused by mutations in an autosomal dominant gene disrupting insulin production. Patients with MODY1 typically develops diabetes (persistent hyperglycemia) before the age of 25 years, but this may not appear until later decades. The degree of insulin deficiency is slowly progressive. Many patients with MODY1 are treated with sulfonylureas for years before insulin is required.

MODY 1 is caused by a loss-of-function mutation in the HNF4α gene. HNF4α is part of a transcription network, including HNF1α (responsible for MODY3) and perhaps HNF1β (MODY5 – see Early Developmental Perturbations in a Human Stem Cell Model of MODY5/HNF1B Pancreatic Hypoplasia), which plays a role in the early development of the pancreas, liver, and intestines. In the pancreas these genes influence the expression of insulin, the principal glucose transporter (GLUT2), and several proteins involved in glucose and mitochondrial metabolism.

We used a combination of global proteomics and cellular biology techniques to investigate the differentiation capacity of insulin-producing cells using a seven-step differentiation protocol (as established by Rezania et al.) of induced pluripotent stem cells, generated from either healthy subjects or MODY1 patients.

Our data show that a human HNF4A mutation is neither blocking the expression of the insulin genes nor the development of insulin-producing cells in vitro. Our analyses also suggest key developmental signalling pathways representing potential targets for improving the efficiency of the current differentiation protocols.

Future studies are required on improving later differentiation stages up to mature insulin-producing β-like cells, which should also reveal the impact of HNF4A-directed transcriptional perturbations on β-cell survival and function.

The paper can be read here.

Probing the missing mature β-cell proteomic landscape in differentiating patient iPSC-derived cells Heidrun Vethe, Yngvild Bjørlykke, Luiza M. Ghila, Joao A. Paulo, Hanne Scholz, Steven P. Gygi, Simona Chera & Helge Ræder
Scientific Reports.2017 Jul 6;7(1):4780. doi: 10.1038/s41598-017-04979-w.

 

New article: Journal of Proteome Research (January 2015)

Patients with carboxyl-ester lipase-maturity-onset diabetes of the young (CEL-MODY) display distinct disease stages toward the development of monogenic diabetes and exocrine pancreatic disease. The finding of differentially increased proteins, some related to MAPK signaling, in a discovery proteomics study of secretin-stimulated duodenal juice in three CEL-MODY patients, prompted us to monitor their abundance in an extensive number of CEL-MODY subjects at different disease stages and controls using targeted proteomics.

Patients with carboxyl-ester lipase-maturity-onset diabetes of the young (CEL-MODY) display distinct disease stages toward the development of monogenic diabetes and exocrine pancreatic disease. The finding of differentially increased proteins, some related to MAPK signaling, in a discovery proteomics study of secretin-stimulated duodenal juice in three CEL-MODY patients, prompted us to monitor their abundance in an extensive number of CEL-MODY subjects at different disease stages and controls using targeted proteomics. In the current study, published in Journal of Proteome Research (January 2015), we demonstrated the feasibility of selected reaction monitoring assays to quantify protein levels in secretin-stimulated duodenal juice. Furthermore, we defined a set of five peptides for potential use as diagnostic tests in CEL-MODY patients. And finally, we proposed a further set of seven proteins with a likely pathogenic role in CEL-MODY disease progression.

The paper can be read here.