A twist code determines the onset of osteoblast differentiation.

By P. Bialek, B. Kern, Xiangli Yang, M. Schrock, Dražen Šošić, N. Hong, Hua Wu, Kai Yu, D. Ornitz, E. Olson and 2 more. Developmental Cell, 2004

703 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f8e7d5ef4b825831de2b7a9380f9885a2ecb4510

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Citations in the corpus

Development of the endochondral skeleton. (2013, background): “Conversely, some other nuclear factors (TWIST1, HAND2, ZFP521, STAT1, Schnurri 3, GLI3, HOXA2, and the HES/HEY proteins) have been found to suppress RUNX2 levels or activity (Kanzler et al. 1998; Kim et al. 2003; Bialek et al. 2004; Garg et al. 2005; Jones et al. 2006; Hilton et al. 2008; Ohba et al”
Histone deacetylase 4 controls chondrocyte hypertrophy during skeletogenesis. (2004, background): “…the Twist-1 and -2 transcription factors were through their association with specific target transcripshown to repress Runx2 activity (Bialek et al., 2004). tion factors suggests possible strategies for therapeutiHowever, the mechanism involved in this form of repres- cally…”
Skeletal remodeling in health and disease (2007, background): “The master transcription regulator for the osteoblast is Runx2, the expression of which is regulated negatively by the transcription factor Twis”
The control of chondrogenesis (2006, background): “The bHLH factor Twist transiently inhibits Runx2 function and prevents premature osteoblast differentiation [Bialek et al., 2004], whereas cooperation of the Groucho homolog Grg5 or the leucine zipper protein ATF4 with Runx2 promotes chondrocyte maturation [Wang et al.”
Review of (2006, background): “A similar developmental regulatory process was recently demonstrated during osteogenesis as the differentiation of osteoblasts is actually determined by the relief of a Runx2-inhibitor twist (Bialek et al., 2004).”
Induction of EMT by twist proteins as a collateral effect of tumor-promoting inactivation of premature senescence. (2008, background): “Interestingly, this phenotype is also found in individuals doubly heterozygous for TWIST1 and TWIST2 alleles, reflecting some functional redundancy (Bialek et al., 2004).”
Canonical Wnt/beta-catenin signaling prevents osteoblasts from differentiating into chondrocytes. (2005, background): “Twist1, which negatively regulates Runx2 activity (Bialek et al., 2004) and is regulated by Wnt/β-catenin signaling in other systems (Borchers et al., 2001; Howe et al., 2003), was downregulated in the mutant like in the wild-type around E14.”
MicroRNA regulation of cell lineages in mouse and human embryonic stem cells. (2008, positive): “Runx2 and Twist1, which are highly expressed in developing bone (Ducy et al., 1997; Bialek et al., 2004), were both upregulated , further supporting our conclusion that mesoderm specification is increased in miR-1-or miR-133-expressing EBs.”
Effects of dexamethasone, ascorbic acid and β-glycerophosphate on the osteogenic differentiation of stem cells in vitro (2013, background): “Bialek and colleagues [45] demonstrated that Twist proteins have an anti-osteogenic function that is mediated by the Twist box, which interacts with the Runx2 DNA-binding domain to inhibit its function in mice.”
Regulation of osteoblast differentiation by transcription factors (2006, background): “Twist proteins interact with Runx2 and inhibit osteoblast differentiation at an early stage [Bialek et al., 2004].”
Mechanical control of stem cell differentiation (2008, background): “The first example is Twist, a basic-helix-loop-helix domain protein, associated with regulation of skeletal development (Bialek et al. 2004; El Ghouzzi et al., 1997; Howard et al., 1997).”