Summary: Sclerostin (SOST)
This is the Wikipedia entry entitled "Sclerostin". More...
The Wikipedia text that you see displayed here is a download from Wikipedia. This means that the information we display is a copy of the information from the Wikipedia database. The button next to the article title ("Edit Wikipedia article") takes you to the edit page for the article directly within Wikipedia. You should be aware you are not editing our local copy of this information. Any changes that you make to the Wikipedia article will not be displayed here until we next download the article from Wikipedia. We currently download new content on a nightly basis.
Does Pfam agree with the content of the Wikipedia entry ?
Pfam has chosen to link families to Wikipedia articles. In some case we have created or edited these articles but in many other cases we have not made any direct contribution to the content of the article. The Wikipedia community does monitor edits to try to ensure that (a) the quality of article annotation increases, and (b) vandalism is very quickly dealt with. However, we would like to emphasise that Pfam does not curate the Wikipedia entries and we cannot guarantee the accuracy of the information on the Wikipedia page.
Editing Wikipedia articles
Before you edit for the first time
Wikipedia is a free, online encyclopedia. Although anyone can edit or contribute to an article, Wikipedia has some strong editing guidelines and policies, which promote the Wikipedia standard of style and etiquette. Your edits and contributions are more likely to be accepted (and remain) if they are in accordance with this policy.
You should take a few minutes to view the following pages:
How your contribution will be recorded
Anyone can edit a Wikipedia entry. You can do this either as a new user or you can register with Wikipedia and log on. When you click on the "Edit Wikipedia article" button, your browser will direct you to the edit page for this entry in Wikipedia. If you are a registered user and currently logged in, your changes will be recorded under your Wikipedia user name. However, if you are not a registered user or are not logged on, your changes will be logged under your computer's IP address. This has two main implications. Firstly, as a registered Wikipedia user your edits are more likely seen as valuable contribution (although all edits are open to community scrutiny regardless). Secondly, if you edit under an IP address you may be sharing this IP address with other users. If your IP address has previously been blocked (due to being flagged as a source of 'vandalism') your edits will also be blocked. You can find more information on this and creating a user account at Wikipedia.
If you have problems editing a particular page, contact us at email@example.com and we will try to help.
The community annotation is a new facility of the Pfam web site. If you have problems editing or experience problems with these pages please contact us.
Sclerostin Edit Wikipedia article
NMR structure of mouse sclerostin.
|Symbols||; CDD; SOST1; VBCH|
Sclerostin is a secreted glycoprotein with a C-terminal cysteine knot-like (CTCK) domain and sequence similarity to the DAN (differential screening-selected gene aberrative in neuroblastoma) family of bone morphogenetic protein (BMP) antagonists. Sclerostin is produced by the osteocyte and has anti-anabolic effects on bone formation.
Sclerostin, the product of the SOST gene, located on chromosome 17q12–q21 in humans, was originally believed to be a non-classical bone morphogenetic protein (BMP) antagonist. More recently sclerostin has been identified as binding to LRP5/6 receptors and inhibiting the Wnt signaling pathway. The inhibition of the Wnt pathway leads to decreased bone formation. Although the underlying mechanisms are unclear, it is believed that the antagonism of BMP-induced bone formation by sclerostin is mediated by Wnt signaling, but not BMP signaling pathways. Sclerostin is expressed in osteocytes and some chondrocytes and it inhibits bone formation by osteoblasts.
Sclerostin production by osteocytes is inhibited by parathyroid hormone, mechanical loading and cytokines including prostaglandin E2, oncostatin M, cardiotrophin-1 and leukemia inhibitory factor. Sclerostin production is increased by calcitonin. Thus, osteoblast activity is self regulated by a negative feedback system.
Mutations in the gene sclerostin are associated with disorders associated with high bone mass, sclerosteosis and van Buchem disease. Sclerosteosis is an autosomal recessive disorder characterized by bone overgrowth. It was first described in 1958 but given the current name in 1967. Excessive bone formation is most prominent in the skull, mandible and tubular bones. It can cause facial distortion and syndactyly. Increased intracranial pressure can cause sudden death in patients. It is a rare disorder that is most prominent in the Afrikaner population in South Africa (40 patients), but there have also been cases of American and Brazilian families.
van Buchem disease is also an autosomal recessive skeletal disease characterized by bone overgrowth. It was first described in 1955 as "hyperostosis corticalis generalisata familiaris", but was given the current name in 1968. Excessive bone formation is most prominent in the skull, mandible, clavicle, ribs and diaphyses of long bones and bone formation occurs throughout life. It is a very rare condition with about 30 known cases in 2002. In 1967 van Buchem characterized the disease in 15 patients of Dutch origin. Patients with sclerosteosis are distinguished from those with van Buchem disease because they are often taller and have hand malformations.
An antibody for sclerostin is being developed because of the protein’s specificity to bone. Its use has increased bone growth in preclinical trials in osteoporotic rats and monkeys. In a Phase I study, a single dose of anti-sclerostin antibody from Amgen (Romosozumab) increased bone density in the hip and spine in healthy men and postmenopausal women and the drug was well tolerated. In a Phase II trial, one year of the antibody treatment in osteoporotic women increased bone density more than bisphosphonate and teriparatide treatment; it had mild injection side effects. It is expected to be on the market in 2017 and is predicted to be the gold standard in osteoporosis treatment by 2021. In addition, OsteoGeneX is developing small molecule inhibitors of sclerostin.
- PDB 2KD3; Weidauer SE, Schmieder P, Beerbaum M, Schmitz W, Oschkinat H, Mueller TD (February 2009). "NMR structure of the Wnt modulator protein Sclerostin". Biochem. Biophys. Res. Commun. 380 (1): 160–5. doi:10.1016/j.bbrc.2009.01.062. PMID 19166819.
- Brunkow ME, Gardner JC, Van Ness J, Paeper BW, Kovacevich BR, Proll S, Skonier JE, Zhao L, Sabo PJ, Fu Y, Alisch RS, Gillett L, Colbert T, Tacconi P, Galas D, Hamersma H, Beighton P, Mulligan J (Feb 2001). "Bone dysplasia sclerosteosis results from loss of the SOST gene product, a novel cystine knot-containing protein". Am J Hum Genet 68 (3): 577–89. doi:10.1086/318811. PMC 1274471. PMID 11179006.
- Balemans W, Ebeling M, Patel N, Van Hul E, Olson P, Dioszegi M, Lacza C, Wuyts W, Van Den Ende J, Willems P, Paes-Alves AF, Hill S, Bueno M, Ramos FJ, Tacconi P, Dikkers FG, Stratakis C, Lindpaintner K, Vickery B, Foernzler D, Van Hul W (Feb 2001). "Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST)". Hum Mol Genet 10 (5): 537–43. doi:10.1093/hmg/10.5.537. PMID 11181578.
- "Entrez Gene: SOST sclerosteosis".
- Van Bezooijen, R. L.; Papapoulos, S. E.; Hamdy, N. A.; Ten Dijke, P.; Löwik, C. W. (2005). "Control of bone formation by osteocytes? Lessons from the rare skeletal disorders sclerosteosis and van Buchem disease". BoneKEy-Osteovision 2 (12): 33. doi:10.1138/20050189.
- Winkler DG, Sutherland MK, Geoghegan JC, Yu C, Hayes T, Skonier JE, Shpektor D, Jonas M, Kovacevich BR, Staehling-Hampton K, Appleby M, Brunkow ME, Latham JA (December 2003). "Osteocyte control of bone formation via sclerostin, a novel BMP antagonist". EMBO J. 22 (23): 6267–76. doi:10.1093/emboj/cdg599. PMC 291840. PMID 14633986.
- Li X, Zhang Y, Kang H, Liu W, Liu P, Zhang J, Harris SE, Wu D (May 2005). "Sclerostin binds to LRP5/6 and antagonizes canonical Wnt signaling". J. Biol. Chem. 280 (20): 19883–7. doi:10.1074/jbc.M413274200. PMID 15778503.
- Ellies DL, Viviano B, McCarthy J, Rey JP, Itasaki N, Saunders S, Krumlauf R (November 2006). "Bone density ligand, Sclerostin, directly interacts with LRP5 but not LRP5G171V to modulate Wnt activity". J. Bone Miner. Res. 21 (11): 1738–49. doi:10.1359/jbmr.060810. PMID 17002572.
- van Bezooijen RL, Svensson JP, Eefting D, Visser A, van der Horst G, Karperien M, Quax PH, Vrieling H, Papapoulos SE, ten Dijke P, Löwik CW (January 2007). "Wnt but not BMP signaling is involved in the inhibitory action of sclerostin on BMP-stimulated bone formation". J. Bone Miner. Res. 22 (1): 19–28. doi:10.1359/jbmr.061002. PMID 17032150.
- Krause C, Korchynskyi O, de Rooij K, Weidauer SE, de Gorter DJ, van Bezooijen RL, Hatsell S, Economides AN, Mueller TD, Löwik CW, ten Dijke P (December 2010). "Distinct modes of inhibition by sclerostin on bone morphogenetic protein and Wnt signaling pathways". J. Biol. Chem. 285 (53): 41614–26. doi:10.1074/jbc.M110.153890. PMC 3009889. PMID 20952383.
- Bonewald LF (February 2011). "The amazing osteocyte". J. Bone Miner. Res. 26 (2): 229–38. doi:10.1002/jbmr.320. PMC 3179345. PMID 21254230.
- Burgers TA, Williams BO (June 2013). "Regulation of Wnt/β-catenin signaling within and from osteocytes". Bone 54 (2): 244–9. doi:10.1016/j.bone.2013.02.022. PMID 23470835.
- Bellido T, Saini V, Pajevic PD (June 2013). "Effects of PTH on osteocyte function". Bone 54 (2): 250–7. doi:10.1016/j.bone.2012.09.016. PMC 3552098. PMID 23017659.
- Bellido T, Ali AA, Gubrij I, Plotkin LI, Fu Q, O'Brien CA, Manolagas SC, Jilka RL (November 2005). "Chronic elevation of parathyroid hormone in mice reduces expression of sclerostin by osteocytes: a novel mechanism for hormonal control of osteoblastogenesis". Endocrinology 146 (11): 4577–83. doi:10.1210/en.2005-0239. PMID 16081646.
- Robling AG, Niziolek PJ, Baldridge LA, Condon KW, Allen MR, Alam I, Mantila SM, Gluhak-Heinrich J, Bellido TM, Harris SE, Turner CH (February 2008). "Mechanical stimulation of bone in vivo reduces osteocyte expression of Sost/sclerostin". J. Biol. Chem. 283 (9): 5866–75. doi:10.1074/jbc.M705092200. PMID 18089564.
- Genetos DC, Yellowley CE, Loots GG (March 2011). "Prostaglandin E2 signals through PTGER2 to regulate sclerostin expression". PLoS ONE 16 (6): e17772. doi:10.1371/journal.pone.0017772. PMC 3059227. PMID 21436889.
- Walker EC, McGregor NE, Poulton IJ, Solano M, Pompolo S, Fernandes TJ, Constable MJ, Nicholson GC, Zhang JG, Nicola NA, Gillespie MT, Martin TJ, Sims NA (February 2010). "Oncostatin M promotes bone formation independently of resorption when signaling through leukemia inhibitory factor receptor in mice.". Journal of Clinical Investigation 120 (2): 582–92. doi:10.1172/JCI40568. PMC 2810087. PMID 20051625.
- Gooi JH, Pompolo S, Karsdal MA, Kulkarni NH, Kalajzic I, McAhren SH, Han B, Onyia JE, Ho PW, Gillespie MT, Walsh NC, Chia LY, Quinn JM, Martin TJ, Sims NA (February 2010). "Calcitonin impairs the anabolic effect of PTH in young rats and stimulates expression of sclerostin by osteocytes.". Bone 46 (6): 1486–97. doi:10.1016/j.bone.2010.02.018. PMID 20188226.
- Balemans, W.; Ebeling, M.; Patel, N.; Van Hul, E.; Olson, P.; Dioszegi, M.; Lacza, C.; Wuyts, W.; Van Den Ende, J.; Willems, P.; Paes-Alves, A. F.; Hill, S.; Bueno, M.; Ramos, F. J.; Tacconi, P.; Dikkers, F. G.; Stratakis, C.; Lindpaintner, K.; Vickery, B.; Foernzler, D.; Van Hul, W. (2001). "Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST)". Human molecular genetics 10 (5): 537–543. doi:10.1093/hmg/10.5.537. PMID 11181578.
- Truswell, A. S. (1958). "Osteopetrosis with syndactyly; a morphological variant of Albers-Schönberg's disease". The Journal of bone and joint surgery. British volume 40–B (2): 209–218. PMID 13539104.
- Balemans, W.; Patel, N.; Ebeling, M.; Van Hul, E.; Wuyts, W.; Lacza, C.; Dioszegi, M.; Dikkers, F. G.; Hildering, P.; Willems, P. J.; Verheij, J. B.; Lindpaintner, K.; Vickery, B.; Foernzler, D.; Van Hul, W. (2002). "Identification of a 52 kb deletion downstream of the SOST gene in patients with van Buchem disease". Journal of medical genetics 39 (2): 91–97. doi:10.1136/jmg.39.2.91. PMC 1735035. PMID 11836356.
- Fosmoe, R. J.; Holm, R. S.; Hildreth, R. C. (1968). "Van Buchem's disease (hyperostosis corticalis generalisata familiaris). A case report". Radiology 90 (4): 771–774. doi:10.1148/90.4.771. PMID 4867898.
- Li, X.; Ominsky, M. S.; Warmington, K. S.; Morony, S.; Gong, J.; Cao, J.; Gao, Y.; Shalhoub, V.; Tipton, B.; Haldankar, R.; Chen, Q.; Winters, A.; Boone, T.; Geng, Z.; Niu, Q. T.; Ke, H. Z.; Kostenuik, P. J.; Simonet, W. S.; Lacey, D. L.; Paszty, C. (2009). "Sclerostin Antibody Treatment Increases Bone Formation, Bone Mass, and Bone Strength in a Rat Model of Postmenopausal Osteoporosis*". Journal of Bone and Mineral Research 24 (4): 578–588. doi:10.1359/jbmr.081206. PMID 19049336.
- Ominsky, M. S.; Vlasseros, F.; Jolette, J.; Smith, S. Y.; Stouch, B.; Doellgast, G.; Gong, J.; Gao, Y.; Cao, J.; Graham, K.; Tipton, B.; Cai, J.; Deshpande, R.; Zhou, L.; Hale, M. D.; Lightwood, D. J.; Henry, A. J.; Popplewell, A. G.; Moore, A. R.; Robinson, M. K.; Lacey, D. L.; Simonet, W. S.; Paszty, C. (2010). "Two doses of sclerostin antibody in cynomolgus monkeys increases bone formation, bone mineral density, and bone strength". Journal of Bone and Mineral Research 25 (5): 948–959. doi:10.1002/jbmr.14. PMID 20200929.
- Padhi, D.; Jang, G.; Stouch, B.; Fang, L.; Posvar, E. (2011). "Single-dose, placebo-controlled, randomized study of AMG 785, a sclerostin monoclonal antibody". Journal of Bone and Mineral Research 26 (1): 19–26. doi:10.1002/jbmr.173. PMID 20593411.
- Reid, I. R. (2012). "Osteoporosis treatment at ASBMR 2012". IBMS BoneKEy 9. doi:10.1038/bonekey.2012.245.
- "For Osteoporosis and Osteopenia, Clinical Data and Thought Leaders' Opinions Indicate that AMG-785/CDP-7851 and Odanacatib Have Advantages Over Alendronate". PR Newswire. 2013-04-04. Retrieved 2013-04-20.
- Rey JP, Ellies DL (January 2010). "Wnt modulators in the biotech pipeline". Dev. Dyn. 239 (1): 102–14. doi:10.1002/dvdy.22181. PMC 3111251. PMID 20014100.
- Balemans W, Van Hul W (2007). "Human genetics of SOST.". Journal of musculoskeletal & neuronal interactions 6 (4): 355–6. PMID 17185822.
- Balemans W, Patel N, Ebeling M, et al. (2002). "Identification of a 52 kb deletion downstream of the SOST gene in patients with van Buchem disease.". J. Med. Genet. 39 (2): 91–7. doi:10.1136/jmg.39.2.91. PMC 1735035. PMID 11836356.
- Staehling-Hampton K, Proll S, Paeper BW, et al. (2002). "A 52-kb deletion in the SOST-MEOX1 intergenic region on 17q12-q21 is associated with van Buchem disease in the Dutch population.". Am. J. Med. Genet. 110 (2): 144–52. doi:10.1002/ajmg.10401. PMID 12116252.
- Balemans W, Foernzler D, Parsons C, et al. (2003). "Lack of association between the SOST gene and bone mineral density in perimenopausal women: analysis of five polymorphisms.". Bone 31 (4): 515–9. doi:10.1016/S8756-3282(02)00844-X. PMID 12398949.
- Strausberg RL, Feingold EA, Grouse LH, et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences.". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMC 139241. PMID 12477932.
- Clark HF, Gurney AL, Abaya E, et al. (2003). "The secreted protein discovery initiative (SPDI), a large-scale effort to identify novel human secreted and transmembrane proteins: a bioinformatics assessment.". Genome Res. 13 (10): 2265–70. doi:10.1101/gr.1293003. PMC 403697. PMID 12975309.
- Sevetson B, Taylor S, Pan Y (2004). "Cbfa1/RUNX2 directs specific expression of the sclerosteosis gene (SOST).". J. Biol. Chem. 279 (14): 13849–58. doi:10.1074/jbc.M306249200. PMID 14739291.
- van Bezooijen RL, Roelen BA, Visser A, et al. (2004). "Sclerostin is an osteocyte-expressed negative regulator of bone formation, but not a classical BMP antagonist.". J. Exp. Med. 199 (6): 805–14. doi:10.1084/jem.20031454. PMC 2212719. PMID 15024046.
- Winkler DG, Yu C, Geoghegan JC, et al. (2004). "Noggin and sclerostin bone morphogenetic protein antagonists form a mutually inhibitory complex.". J. Biol. Chem. 279 (35): 36293–8. doi:10.1074/jbc.M400521200. PMID 15199066.
- Zhang Z, Henzel WJ (2005). "Signal peptide prediction based on analysis of experimentally verified cleavage sites.". Protein Sci. 13 (10): 2819–24. doi:10.1110/ps.04682504. PMC 2286551. PMID 15340161.
- Sutherland MK, Geoghegan JC, Yu C, et al. (2005). "Sclerostin promotes the apoptosis of human osteoblastic cells: a novel regulation of bone formation.". Bone 35 (4): 828–35. doi:10.1016/j.bone.2004.05.023. PMID 15454089.
- Gerhard DS, Wagner L, Feingold EA, et al. (2004). "The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).". Genome Res. 14 (10B): 2121–7. doi:10.1101/gr.2596504. PMC 528928. PMID 15489334.
- Uitterlinden AG, Arp PP, Paeper BW, et al. (2005). "Polymorphisms in the sclerosteosis/van Buchem disease gene (SOST) region are associated with bone-mineral density in elderly whites.". Am. J. Hum. Genet. 75 (6): 1032–45. doi:10.1086/426458. PMC 1182139. PMID 15514891.
- Winkler DG, Sutherland MS, Ojala E, et al. (2005). "Sclerostin inhibition of Wnt-3a-induced C3H10T1/2 cell differentiation is indirect and mediated by bone morphogenetic proteins.". J. Biol. Chem. 280 (4): 2498–502. doi:10.1074/jbc.M400524200. PMID 15545262.
- Poole KE, van Bezooijen RL, Loveridge N, et al. (2006). "Sclerostin is a delayed secreted product of osteocytes that inhibits bone formation.". FASEB J. 19 (13): 1842–4. doi:10.1096/fj.05-4221fje. PMID 16123173.
- Gardner JC, van Bezooijen RL, Mervis B, et al. (2006). "Bone mineral density in sclerosteosis; affected individuals and gene carriers.". J. Clin. Endocrinol. Metab. 90 (12): 6392–5. doi:10.1210/jc.2005-1235. PMID 16189254.
Sclerostin (SOST) Provide feedback
This family contains several mammalian sclerostin (SOST) proteins. SOST is thought to suppress bone formation. Mutations of the SOST gene lead to sclerosteosis, a progressive sclerosing bone dysplasia with an autosomal recessive mode of inheritance. Radiologically, it is characterised by a generalised hyperostosis and sclerosis leading to a markedly thickened and sclerotic skull, with mandible, ribs, clavicles and all long bones also being affected. Due to narrowing of the foramina of the cranial nerves, facial nerve palsy, hearing loss and atrophy of the optic nerves can occur. Sclerosteosis is clinically and radiologically very similar to van Buchem disease, mainly differentiated by hand malformations and a large stature in sclerosteosis patients .
Balemans W, Ebeling M, Patel N, Van Hul E, Olson P, Dioszegi M, Lacza C, Wuyts W, Van Den Ende J, Willems P, Paes-Alves AF, Hill S, Bueno M, Ramos FJ, Tacconi P, Dikkers FG, Stratakis C, Lindpaintner K, Vickery B, Foernzler D, Van Hul W; , Hum Mol Genet 2001;10:537-543.: Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST). PUBMED:11181578 EPMC:11181578
Brunkow ME, Gardner JC, Van Ness J, Paeper BW, Kovacevich BR, Proll S, Skonier JE, Zhao L, Sabo PJ, Fu Y, Alisch RS, Gillett L, Colbert T, Tacconi P, Galas D, Hamersma H, Beighton P, Mulligan J; , Am J Hum Genet 2001;68:577-589.: Bone dysplasia sclerosteosis results from loss of the SOST gene product, a novel cystine knot-containing protein. PUBMED:11179006 EPMC:11179006
External database links
This tab holds annotation information from the InterPro database.
InterPro entry IPR008835This sclerostin family consists of sclerostin and sclerostin domain-containing protein 1. Sclerostin (SOST) is thought to suppress bone formation. Mutations of the SOST gene lead to sclerosteosis, a progressive sclerosing bone dysplasia with an autosomal recessive mode of inheritance. Radiologically, it is characterised by a generalised hyperostosis and sclerosis leading to a markedly thickened and sclerotic skull, with mandible, ribs, clavicles and all long bones also being affected. Due to narrowing of the foramina of the cranial nerves, facial nerve palsy, hearing loss and atrophy of the optic nerves can occur. Sclerosteosis is clinically and radiologically very similar to van Buchem disease, mainly differentiated by hand malformations and a large stature in sclerosteosis patients [PUBMED:11181578]. Sclerostin domain-containing protein 1, also known as USAG1, is a bone morphogenetic protein antagonist [PUBMED:15020244].
|Cellular component||extracellular space (GO:0005615)|
- the number of sequences which exhibit this architecture
a textual description of the architecture, e.g. Gla, EGF x 2, Trypsin.
This example describes an architecture with one
Gladomain, followed by two consecutive
EGFdomains, and finally a single
- the UniProt description of the protein sequence
- the number of residues in the sequence
- the Pfam graphic itself.
Loading domain graphics...
The cytokine families in this clan have the cystine-knot fold. In this 6 cysteines form three disulphide bridges that are interlinked.
The clan contains the following 9 members:Coagulin Cys_knot DAN Hormone_6 NGF Noggin PDGF Sclerostin TGF_beta
We make a range of alignments for each Pfam-A family:
- the curated alignment from which the HMM for the family is built
- the alignment generated by searching the sequence database using the HMM
- Representative Proteomes (RPs) at 15%, 35%, 55% and 75% co-membership thresholds
- alignment generated by searching the NCBI sequence database using the family HMM
- alignment generated by searching the metagenomics sequence database using the family HMM
You can see the alignments as HTML or in three different sequence viewers:
- Pfam viewer
- an HTML-based viewer that uses DAS to retrieve alignment fragments on request
1Cannot generate PP/Heatmap alignments for seeds; no PP data available
Key: available, not generated, — not available.
Format an alignment
If you find these logos useful in your own work, please consider citing the following article:
Note: You can also download the data file for the tree.
Curation and family details
|Seed source:||Pfam-B_16740 (release 8.0)|
|Number in seed:||4|
|Number in full:||114|
|Average length of the domain:||177.90 aa|
|Average identity of full alignment:||50 %|
|Average coverage of the sequence by the domain:||95.52 %|
|HMM build commands:||
build method: hmmbuild -o /dev/null HMM SEED
search method: hmmsearch -Z 23193494 -E 1000 --cpu 4 HMM pfamseq
|Family (HMM) version:||6|
|Download:||download the raw HMM for this family|
Weight segments by...
Change the size of the sunburst
selected sequences to HMM
a FASTA-format file
- 0 sequences
- 0 species
How the sunburst is generated
Colouring and labels
Anomalies in the taxonomy tree
Missing taxonomic levels
Unmapped species names
Too many species/sequences
The tree shows the occurrence of this domain across different species. More...
You can use the tree controls to manipulate how the interactive tree is displayed:
- show/hide the summary boxes
- highlight species that are represented in the seed alignment
- expand/collapse the tree or expand it to a given depth
- select a sub-tree or a set of species within the tree and view them graphically or as an alignment
- save a plain text representation of the tree
For those sequences which have a structure in the Protein DataBank, we use the mapping between UniProt, PDB and Pfam coordinate systems from the PDBe group, to allow us to map Pfam domains onto UniProt sequences and three-dimensional protein structures. The table below shows the structures on which the Sclerostin domain has been found. There are 3 instances of this domain found in the PDB. Note that there may be multiple copies of the domain in a single PDB structure, since many structures contain multiple copies of the same protein seqence.
Loading structure mapping...