Pkcδ Is Required for Jagged-1 Induction of hMSC Osteogenic Differentiation.
Philadelphia, United States. In Stem Cells, 13 Mar 2013
Overexpression of the notch-2 intracellular domain (NICD) is sufficient to mimic the effect of Jag1 on hMSC osteoblastogenesis, while blocking Notch signaling with a gamma-secretase inhibitor or with dominant negative mastermind inhibits Jag1 induced hMSC osteoblastogenesis.
Notch signaling in human development and disease.
Philadelphia, United States. In Semin Cell Dev Biol, Jun 2012
Notch associated disorders include the autosomal dominant, multi-system, Alagille syndrome caused by mutations in both a ligand (Jagged1 (JAG1)) and receptor (NOTCH2) and autosomal recessive spondylocostal dysostosis, caused by mutations in a ligand (Delta-like-3 (DLL3)), as well as several other members of the Notch signaling pathway.
Alagille syndrome: pathogenesis, diagnosis and management.
Exeter, United Kingdom. In Eur J Hum Genet, Mar 2012
Alagille syndrome (ALGS), also known as arteriohepatic dysplasia, is a multisystem disorder due to defects in components of the Notch signalling pathway, most commonly due to mutation in JAG1 (ALGS type 1), but in a small proportion of cases mutation in NOTCH2 (ALGS type 2).
Control and interference in task switching--a review.
Würzburg, Germany. In Psychol Bull, 2010
We consider preparation processes in two-stage models, consider preparation as an all-or-none process, address the question of whether preparation is switch-specific, reflect on preparation as interaction of cue encoding and memory retrieval, and discuss the impact of verbal mediation on preparation.
The role of inhibition in task switching: a review.
Aachen, Germany. In Psychon Bull Rev, 2010
n-2 repetition costs refer to the performance impairment in sequences of the ABA type relative to CBA, which can be interpreted in terms of persisting inhibition of previously abandoned tasks.
Clinical risk factors, DNA variants, and the development of type 2 diabetes.
Malmö, Sweden. In N Engl J Med, 2008
Variants in 11 genes (TCF7L2, PPARG, FTO, KCNJ11, NOTCH2, WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX) were significantly associated with the risk of type 2 diabetes independently of clinical risk factors; variants in 8 of these genes were associated with impaired beta-cell function.