Target type: biologicalprocess
The process in which any suture between cranial and/or facial bones is generated and organized. [GOC:pr, GOC:sl, Wikipedia:Cranial_sutures, Wikipedia:Head_and_neck_anatomy#Musculoskeletal_system]
Craniofacial suture morphogenesis is a complex developmental process that involves the coordinated interaction of multiple cell types and signaling pathways. It begins early in embryonic development and continues throughout infancy and childhood, ultimately shaping the skull and facial bones.
The sutures are fibrous joints that separate the bones of the skull. They are essential for allowing the skull to grow and accommodate the developing brain. During suture formation, mesenchymal cells differentiate into osteoblasts, which deposit bone matrix. The osteoblasts are organized into layers, with the outermost layer being responsible for bone formation and the innermost layer being responsible for bone resorption.
The precise regulation of bone formation and resorption within the suture is crucial for normal skull development. A variety of factors, including genetic, epigenetic, and environmental influences, can affect suture morphogenesis.
Here are some key aspects of craniofacial suture morphogenesis:
* **Formation:** The sutures form during embryonic development from mesenchymal tissue. The mesenchymal cells differentiate into osteoblasts, which deposit bone matrix.
* **Growth:** The sutures grow throughout infancy and childhood, allowing the skull to expand as the brain grows. This growth occurs by the coordinated action of osteoblasts and osteoclasts.
* **Fusion:** The sutures eventually fuse, typically in late adolescence or early adulthood. This fusion is a gradual process, and the timing of fusion can vary depending on the suture.
* **Regulation:** The morphogenesis of the sutures is regulated by a complex interplay of signaling pathways, including the Wnt, BMP, and FGF pathways. These pathways influence cell proliferation, differentiation, and bone formation.
Disruptions in craniofacial suture morphogenesis can lead to various craniofacial abnormalities, such as craniosynostosis (premature fusion of the sutures), plagiocephaly (deformation of the skull), and facial asymmetry. Understanding the complex mechanisms that underlie suture development is essential for diagnosing and treating these conditions.'
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Protein | Definition | Taxonomy |
---|---|---|
Matrix metalloproteinase-16 | A matrix metalloproteinase-16 that is encoded in the genome of human. [PRO:DNx, UniProtKB:P51512] | Homo sapiens (human) |
Matrix metalloproteinase-14 | A matrix metalloproteinase-14 that is encoded in the genome of human. [PRO:DNx, UniProtKB:P50281] | Homo sapiens (human) |
Compound | Definition | Classes | Roles |
---|---|---|---|
tiludronic acid | tiludronic acid: a bone resorption inhibitor; an antihypercalcemic agent; used in the tratment of Paget's disease; used in the treatment and prevention of osteoporosis; structure given in first source | organochlorine compound | |
epigallocatechin gallate | (-)-epigallocatechin 3-gallate : A gallate ester obtained by the formal condensation of gallic acid with the (3R)-hydroxy group of (-)-epigallocatechin. epigallocatechin gallate: a steroid 5alpha-reductase inhibitor and antimutagen in green tea (Camellia sinensis) | flavans; gallate ester; polyphenol | antineoplastic agent; antioxidant; apoptosis inducer; geroprotector; Hsp90 inhibitor; neuroprotective agent; plant metabolite |
zoledronic acid | zoledronic acid : An imidazole compound having a 2,2-bis(phosphono)-2-hydroxyethane-1-yl substituent at the 1-position. Zoledronic Acid: An imidobisphosphonate inhibitor of BONE RESORPTION that is used for the treatment of malignancy-related HYPERCALCEMIA; OSTEITIS DEFORMANS; and OSTEOPOROSIS. | 1,1-bis(phosphonic acid); imidazoles | bone density conservation agent |
marimastat | marimastat : A secondary carboxamide resulting from the foraml condensation of the carboxy group of (2R)-2-[(1S)-1-hydroxy-2-(hydroxyamino)-2-oxoethyl]-4-methylpentanoic acid with the alpha-amino group of N,3-dimethyl-L-valinamide. marimastat: a matrix metalloproteinase inhibitor active in patients with advanced carcinoma of the pancreas, prostate, or ovary | hydroxamic acid; secondary carboxamide | antineoplastic agent; matrix metalloproteinase inhibitor |
ilomastat | CS 610: matrix metalloproteinase inhibitor; structure in first source ilomastat : An N-acyl-amino acid obtained by formal condensation of the carboxy group of (2R)-2-[2-(hydroxyamino)-2-oxoethyl]-4-methylpentanoic acid with the amino group of N-methyl-L-tryptophanamide. A cell permeable broad-spectrum matrix metalloproteinase (MMP) inhibitor | hydroxamic acid; L-tryptophan derivative; N-acyl-amino acid | anti-inflammatory agent; antibacterial agent; antineoplastic agent; EC 3.4.24.24 (gelatinase A) inhibitor; neuroprotective agent |
cgs 27023a | CGS 27023A: a matrix metalloproteinase inhibitor | ||
prinomastat | prinomastat : A hydroxamic acid that is (3S)-N-hydroxy-2,2-dimethylthiomorpholine-3-carboxamide in which the hydrogen attached to the thiomorpholine nitrogen has been replaced by a [4-(pyridin-4-yloxy)phenyl]sulfonyl group. It is a selective inhibitor with of matrix metalloproteinases (MMPs) 2, 3, 9, 13, and 14. prinomastat: a diazepine-based hydroxamic acid inhibitor; matrix metalloproteinase (MMP) inhibitor; angiogenesis inhibitor; | aromatic ether; hydroxamic acid; pyridines; sulfonamide; thiomorpholines | antineoplastic agent; EC 3.4.24.35 (gelatinase B) inhibitor; matrix metalloproteinase inhibitor |
rs-130830 | RS-130830: orally-active broad-spectrum matrix metalloproteinase inhibitor | ||
tmi-1 | |||
batimastat | batimastat : A secondary carboxamide resulting from the formal condensation of the carboxy group of (2S,3R)-5-methyl-3-{[(2S)-1-(methylamino)-1-oxo-3-phenylpropan-2-yl]carbamoyl}-2-[(thiophen-2-ylsulfanyl)methyl]hexanoic acid with the amino group of hydroxylamine. It a broad-spectrum matrix metalloprotease inhibitor. batimastat: structure given in first source; a synthetic matrix metalloproteinase inhibitor | hydroxamic acid; L-phenylalanine derivative; organic sulfide; secondary carboxamide; thiophenes; triamide | angiogenesis inhibitor; antineoplastic agent; matrix metalloproteinase inhibitor |
ik 682 | IK 682: inhibits TNF-alpha converting enzyme; structure in first source | hydroxamic acid; pyrrolidin-2-ones; quinolines | |
epigallocatechin-3-o-(3''-o-methyl)-gallate | catechin | ||
ro 32-3555 | Ro 32-3555: structure given in first source | ||
sb 3ct compound | SB 3CT compound: a matrix metalloproteinase-2 inhibitor; structure in first source | aromatic ether | |
pd 166793 | |||
sc 78080 | |||
ro 31-9790 | Ro 31-9790: hydroxamic acid derivative | ||
arp-100 | |||
kb r8301 | |||
N(2)-([biphenyl]-4-ylsulfonyl)-N-hydroxy-N(2)-isopropoxy-D-valinamide | N(2)-([biphenyl]-4-ylsulfonyl)-N-hydroxy-N(2)-isopropoxy-D-valinamide : A hydroxamic acid that is N-hydroxy-D-valinamide in which the alpha-amino group has been substituted by isopropoxy and [biphenyl]-4-ylsulfonyl groups. A selective matrix metalloproteinase-2 (MMP-2) inhibitor, it is one of the most potent inducers of autophagy. Its physiological roles include angiogenesis, cancer metastasis, embryogenesis, tissue remodeling in development, and wound healing. | D-valine derivative; hydroxamic acid | antineoplastic agent; autophagy inducer; EC 3.4.24.24 (gelatinase A) inhibitor; melanin synthesis inhibitor |
bms-566394 | BMS-566394: structure in first source | ||
incb3619 | INCB3619: ADAM inhibitor; structure in first source | ||
6-(3,5-difluoroanilino)-9-ethyl-2-purinecarbonitrile | 6-aminopurines | ||
6-(3,5-difluoroanilino)-9-(2,2-difluoroethyl)-2-purinecarbonitrile | 6-aminopurines | ||
9-(3,5-difluorophenyl)-6-(ethylamino)-2-purinecarbonitrile | imidazoles | ||
grassystatin a | grassystatin A: isolated from a cyanobacterium, identified as Lyngbya cf.; structure in first source |