This will be one of the shorter posts.
It is almost been completely concluded that the glycoprotein Noggin and the gene that creates inhibits longitudinal growth. Mutations in the gene often leads to tall stature.
from the wikipedia article on Noggin (HERE)
Noggin, also known as NOG, is a protein which in humans is encoded by the NOG gene.
Noggin inhibits TGF-β signal transduction by binding to TGF-β family ligands and preventing them from binding to their corresponding receptors. Noggin plays a key role in neural induction by inhibiting BMP4, along with other TGF-β signaling inhibitors such as chordin and follistatin. Mouse knockout experiments have demonstrated that noggin also plays a crucial role in bone development, joint formation, and neural tube fusion
The secreted polypeptide noggin, encoded by the NOG gene, binds and inactivates members of the transforming growth factor-beta (TGF-beta) superfamily signaling proteins, such as bone morphogenetic protein-4 (BMP4). By diffusing through extracellular matrices more efficiently than members of the TGF-beta superfamily, noggin may have a principal role in creating morphogenic gradients. Noggin appears to have pleiotropic effect, both early in development as well as in later stages. The results of the mouse knockout of noggin suggest that it is involved in numerous developmental processes, such as neural tube fusion and joint formation.
From HeightQuest they also mention that Noggin inhibits the affects of BMPs HERE
From this study HERE…
Horm Res. 2008;69(4):221-6. Epub 2008 Jan 21.
Growth and skeletal development in families with NOGGIN gene mutations.
Department of Paediatric Endocrinology, Royal Hospital for Sick Children, Edinburgh, UK.
There is a scarcity of data on height as well as bone densitometry in humans with NOGGIN mutations.
In 2 families with symphalangism, anthropometry, bone densitometry and genetic analysis of the NOGGIN gene were performed.
In family A, the height standard deviation scores of the affected father and son were -0.4 and 3.5, respectively. In family B, the height standard deviation scores of the affected father, twin daughters and another daughter were 1.7, 1.8, 2.4 and 1.8, respectively. In the children, percentage predicted bone mineral content (BMC) for height at the appendicular sites (total femur, femoral neck) was lower than at an axial site lumbar spine. In the 2 fathers, median bone mineral density at total femur and femoral neck was -0.3 standard deviation scores (-0.7, 0.2) and at lumbar spine the scores were -0.4 and 0.9. The children had median tibial and radial speed of sound velocities of -2.1 (-0.9 to -6.4) and -1.4 (-0.2 to -4.9), respectively. DNA analysis revealed a novel missense mutation in family A and family B, resulting in a Met190Val substitution and a Pro42Arg substitution, respectively.
Heterozygous gene mutations in NOGGIN are associated with tall stature in children but not necessarily in adults. The appendicular BMC and speed of sound may be low in affected children but normalises by adulthood. However, axial BMC seems normal in childhood and is high in adulthood.
(c) 2008 S. Karger AG, Basel
- PMID: 18204269 [PubMed – indexed for MEDLINE]