Sost sclerostin [Rattus norvegicus (Norway rat)] - Gene

Summary

Official Symbol: Sostprovided by RGD
Official Full Name: sclerostinprovided by RGD
Primary source: RGD:69358
See related: Ensembl:ENSRNOG00000071073 AllianceGenome:RGD:69358
Gene type: protein coding
RefSeq status: PROVISIONAL
Organism: Rattus norvegicus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Rattus
Summary: Predicted to enable BMP binding activity. Involved in ossification. Located in Golgi apparatus and extracellular space. Part of protein-containing complex. Human ortholog(s) of this gene implicated in SOST-related sclerosing bone dysplasia; autosomal dominant craniodiaphyseal dysplasia; sclerosteosis; and sclerosteosis 1. Orthologous to human SOST (sclerostin). [provided by Alliance of Genome Resources, Apr 2022]
Expression: Biased expression in Thymus (RPKM 7.8), Spleen (RPKM 7.3) and 6 other tissues See more
Orthologs: human mouse all
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Genomic context

Location:: 10q32.1

Exon count:: 2

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCr8 (GCF_036323735.1)	10	NC_086028.1 (87412722..87415766, complement)
RS_2023_06	previous assembly	mRatBN7.2 (GCF_015227675.2)	10	NC_051345.1 (86912517..86915561, complement)
106	previous assembly	Rnor_6.0 (GCF_000001895.5)	10	NC_005109.4 (89897087..89900131, complement)

Chromosome 10 - NC_086028.1 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Go to reference sequence details

Genomic Sequence:

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Expression

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See details

Project title: A rat RNA-Seq transcriptomic BodyMap across 11 organs and 4 developmental stages
Description: 320 RNA samples isolated from 11 organs (adrenal gland, brain, heart, kidney, liver, lung, muscle, spleen, thymus, and testes or uterus) from both sexes of Fischer 344 rats across four developmental stages (2-, 6-, 21-, and 104-weeks-old)
BioProject: PRJNA238328
Publication: PMID 24510058
Analysis date: Mon Jun 6 17:44:12 2016

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

The Possible Role of Sclerostin in the Pathogenesis of Tympanosclerosis.
Title: The Possible Role of Sclerostin in the Pathogenesis of Tympanosclerosis.
Changes in the intra- and peri-cellular sclerostin distribution in lacuno-canalicular system induced by mechanical unloading.
Title: Changes in the intra- and peri-cellular sclerostin distribution in lacuno-canalicular system induced by mechanical unloading.
Sclerostin as Regulatory Molecule in Vascular Media Calcification and the Bone-Vascular Axis.
Title: Sclerostin as Regulatory Molecule in Vascular Media Calcification and the Bone-Vascular Axis.
The combination of ZOL and the osteoanabolic sclerostin antibody was more effective than either agent alone.
Title: Systemic sclerostin antibody treatment increases osseointegration and biomechanical competence of zoledronic-acid-coated dental implants in a rat osteoporosis model.
More surprisingly SOST and DKK1 were overexpressed from day 6 and followed by a dramatic decrease in bone formation from day 8. At the time of arthritis onset, SOST and DKK1 returned to control values, but frizzled related protein 1 (SFRP1), proinflammatory cytokines, and MMPs started to increase.
Title: Early sclerostin expression explains bone formation inhibition before arthritis onset in the rat adjuvant-induced arthritis model.
beta-GP induced VSMC calcification by activating the Wnt/beta-catenin signaling pathway. Sclerostin and Lrp4 were involved in beta-GP-induced VSMC calcification and play an important role. GBE could alleviate VSMC calcification induced by beta-GP through inhibiting the Wnt/beta-catenin signaling pathway.
Title: Sclerostin/Receptor Related Protein 4 and Ginkgo Biloba Extract Alleviates β-Glycerophosphate-Induced Vascular Smooth Muscle Cell Calcification By Inhibiting Wnt/β-Catenin Pathway.
alleviated the osteogenic differentiation of ectomesenchymal stem cells (EMSCs), and LNGFR enhanced the osteogenic differentiation of EMSCs by decreasing SOST
Title: SOST, an LNGFR target, inhibits the osteogenic differentiation of rat ectomesenchymal stem cells.
TNF-alpha might mediate alveolar bone loss via inducing expression of osteocytic RANKL and sclerostin in type 1 diabetes rats with periodontitis
Title: Tumor necrosis factor-α antagonist diminishes osteocytic RANKL and sclerostin expression in diabetes rats with periodontitis.
Four genes are expressed significantly higher in basal bone than in alveolar bone: SOST, E-11, DMP-1, and MEPE. Three of the proteins (SOST, MEPE, and DMP-1) are associated with mature osteocytes, indicating that basal bone has more mature osteocyte phenotypes because the immature osteocyte converts to a mature osteocyte as a result of bone mineralization.
Title: Inherent physical characteristics and gene expression differences between alveolar and basal bones.
These data suggest that sclerostin plays an important role in the bone remodeling of tooth movement.
Title: Sclerostin Promotes Bone Remodeling in the Process of Tooth Movement.

Submit: New GeneRIF Correction See all GeneRIFs (25)

General gene information

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Gene Ontology Provided by RGD

Function	Evidence Code	Pubs
enables BMP binding	IBA Inferred from Biological aspect of Ancestor more info
enables DNA-binding transcription factor binding	ISO Inferred from Sequence Orthology more info
enables carbohydrate binding	ISO Inferred from Sequence Orthology more info
enables heparin binding	IEA Inferred from Electronic Annotation more info
enables molecular function inhibitor activity	ISO Inferred from Sequence Orthology more info
enables protein binding	IPI Inferred from Physical Interaction more info	PubMed

Process	Evidence Code	Pubs
acts_upstream_of BMP signaling pathway	ISO Inferred from Sequence Orthology more info
acts_upstream_of canonical Wnt signaling pathway	ISO Inferred from Sequence Orthology more info
involved_in cellular response to parathyroid hormone stimulus	ISO Inferred from Sequence Orthology more info
involved_in negative regulation of BMP signaling pathway	IBA Inferred from Biological aspect of Ancestor more info
acts_upstream_of_or_within negative regulation of BMP signaling pathway	ISO Inferred from Sequence Orthology more info
involved_in negative regulation of Wnt signaling pathway	IBA Inferred from Biological aspect of Ancestor more info
acts_upstream_of_or_within negative regulation of Wnt signaling pathway	ISO Inferred from Sequence Orthology more info
acts_upstream_of_or_within negative regulation of canonical Wnt signaling pathway	ISO Inferred from Sequence Orthology more info
involved_in negative regulation of canonical Wnt signaling pathway	ISO Inferred from Sequence Orthology more info
acts_upstream_of_or_within negative regulation of ossification	ISO Inferred from Sequence Orthology more info
involved_in negative regulation of protein-containing complex assembly	ISO Inferred from Sequence Orthology more info
involved_in ossification	IBA Inferred from Biological aspect of Ancestor more info
involved_in ossification	IEP Inferred from Expression Pattern more info	PubMed
acts_upstream_of_or_within ossification	ISO Inferred from Sequence Orthology more info
involved_in positive regulation of DNA-templated transcription	ISO Inferred from Sequence Orthology more info
involved_in response to mechanical stimulus	ISO Inferred from Sequence Orthology more info

Component	Evidence Code	Pubs
located_in Golgi apparatus	IDA Inferred from Direct Assay more info	PubMed
is_active_in extracellular space	IBA Inferred from Biological aspect of Ancestor more info
located_in extracellular space	IDA Inferred from Direct Assay more info	PubMed
part_of protein-containing complex	IDA Inferred from Direct Assay more info	PubMed

General protein information

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Preferred Names: sclerostin

Names: sclerosteosis

NCBI Reference Sequences (RefSeq)

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RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above.