Key features and details
- Rabbit polyclonal to Msx2/Hox8
- Suitable for: IHC-P
- Reacts with: Human
- Isotype: IgG
Product nameAnti-Msx2/Hox8 antibody
See all Msx2/Hox8 primary antibodies
DescriptionRabbit polyclonal to Msx2/Hox8
Tested applicationsSuitable for: IHC-Pmore details
Species reactivityReacts with: Human
Predicted to work with: Cow, Chimpanzee, Gorilla
- IHC-P: Human endometrium, placenta and urinary bladder tissue.
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.20
Preservative: 0.02% Sodium azide
Constituents: 40% Glycerol (glycerin, glycerine), PBS
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab223692 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-P||1/50 - 1/200. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.|
FunctionActs as a transcriptional regulator in bone development. Represses the ALPL promoter activity and antogonizes the stimulatory effect of DLX5 on ALPL expression during osteoblast differentiation. Probable morphogenetic role. May play a role in limb-pattern formation. In osteoblasts, suppresses transcription driven by the osteocalcin FGF response element (OCFRE). Binds to the homeodomain-response element of the ALPL promoter.
Involvement in diseaseDefects in MSX2 are the cause of parietal foramina 1 (PFM1) [MIM:168500]; also known as foramina parietalia permagna (FPP). PFM1 is an autosomal dominant disease characterized by oval defects of the parietal bones caused by deficient ossification around the parietal notch, which is normally obliterated during the fifth fetal month.
Defects in MSX2 are the cause of parietal foramina with cleidocranial dysplasia (PFMCCD) [MIM:168550]; also known as cleidocranial dysplasia with parietal foramina. PFMCCD combines skull defects in the form of enlarged parietal foramina and deficient ossification of the clavicles.
Defects in MSX2 are the cause of craniosynostosis type 2 (CRS2) [MIM:604757]; also known as craniosynostosis Boston-type (CSB). CRS2 is an autosomal dominant disorder characterized by the premature fusion of calvarial sutures. The craniosynostosis phenotype is either fronto-orbital recession, or frontal bossing, or turribrachycephaly, or cloverleaf skull. Associated features include severe headache, high incidence of visual problems (myopia or hyperopia), and short first metatarsals. Intelligence is normal.
Sequence similaritiesBelongs to the Msh homeobox family.
Contains 1 homeobox DNA-binding domain.
- Information by UniProt
- CRS 2 antibody
- CRS2 antibody
- FPP antibody
Formalin-fixed, paraffin-embedded human endometrium tissue stained for Msx2/Hox8 using ab223692 at 1/50 dilution in immunohistochemical analysis.
Formalin-fixed, paraffin-embedded human placenta tissue stained for Msx2/Hox8 using ab223692 at 1/50 dilution in immunohistochemical analysis.
Formalin-fixed, paraffin-embedded human urinary bladder tissue stained for Msx2/Hox8 using ab223692 at 1/50 dilution in immunohistochemical analysis.
Formalin-fixed, paraffin-embedded human endometrium tissue stained for Msx2/Hox8 using ab223692 at 1/50 dilution in immunohistochemical analysis. Low positivity, as expected.
ab223692 has been referenced in 4 publications.
- Cai C et al. Msx2 plays an important role in BMP6-induced osteogenic differentiation of two mesenchymal cell lines: C3H10T1/2 and C2C12. Regen Ther 14:245-251 (2020). PubMed: 32455154
- Wang C et al. Poly(ADP-ribose) polymerase 1 accelerates vascular calcification by upregulating Runx2. Nat Commun 10:1203 (2019). PubMed: 30867423
- Li Y et al. CTRP13 attenuates vascular calcification by regulating Runx2. FASEB J 33:9627-9637 (2019). PubMed: 31145871
- Jiang Y et al. Histological study of postnatal development of mouse tongues. Exp Ther Med 15:383-386 (2018). PubMed: 29375694