Development of the Endochondral Skeleton
Citations
981 citations
566 citations
337 citations
333 citations
312 citations
References
5,834 citations
"Development of the Endochondral Ske..." refers background in this paper
...NOTCH signaling mediates communication between neighboring cells to control cell fate decisions in all metazoans (Artavanis-Tsakonas et al. 1999; Chiba 2006)....
[...]
4,196 citations
"Development of the Endochondral Ske..." refers background in this paper
...Homozygous deletion of RUNX2 or its nuclear targeting signal in mice resulted in a complete lack of osteoblasts (Komori et al. 1997; Otto et al. 1997), whereas haploinsufficiency of RUNX2 in either mice or humans causes cleidocranial dysplasia (Lee et al. 1997; Mundlos et al. 1997; Choi et al.…...
[...]
...Homozygous deletion of RUNX2 or its nuclear targeting signal in mice resulted in a complete lack of osteoblasts (Komori et al. 1997; Otto et al. 1997), whereas haploinsufficiency of RUNX2 in either mice or humans causes cleidocranial dysplasia (Lee et al....
[...]
...Interestingly, in the absence of RUNX2, the perichondrium (normally containing osteogenic progenitors) becomes hypoplastic (Komori et al. 1997; Otto et al. 1997), indicating that RUNX2 may be necessary for the production and/or maintenance of the progenitors....
[...]
3,283 citations
"Development of the Endochondral Ske..." refers background in this paper
...Deletion of OSX results in a complete absence of osteoblasts in the mouse embryo, even though expression of RUNX2 is relatively normal (Nakashima et al. 2002)....
[...]
...These results, together with the observation that Osx expression is abolished in Runx2 – / – mice (Nakashima et al. 2002), indicate that OSX functions downstream from RUNX2 as another indispensable regulator of osteoblast differentiation....
[...]
...…leads to a hypoplastic perichondrium, loss of OSX causes ectopic cartilage formation beneath a thickened perichondrium at the midshaft of long bones (where a bone collar normally forms), possibly because of a fate switch of progenitors from osteoblasts to chondrocytes (Nakashima et al. 2002)....
[...]
...Whereas RUNX2 deletion leads to a hypoplastic perichondrium, loss of OSX causes ectopic cartilage formation beneath a thickened perichondrium at the midshaft of long bones (where a bone collar normally forms), possibly because of a fate switch of progenitors from osteoblasts to chondrocytes (Nakashima et al. 2002)....
[...]
3,120 citations
2,919 citations