Key features and details
- Rabbit polyclonal to Msx2/Hox8 - N-terminal
- Suitable for: WB, IHC-P
- Reacts with: Human
- Isotype: IgG
Product nameAnti-Msx2/Hox8 antibody - N-terminal
See all Msx2/Hox8 primary antibodies
DescriptionRabbit polyclonal to Msx2/Hox8 - N-terminal
Tested applicationsSuitable for: WB, IHC-Pmore details
Species reactivityReacts with: Human
Synthetic peptide corresponding to Human Msx2/Hox8 (N terminal) conjugated to Keyhole Limpet Haemocyanin (KLH). NP_002440.2.
Database link: P35548
- Human skin tissue; 293 cell lysates transiently transfected with the Msx2/Hox8 gene.
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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 bufferPreservative: 0.09% Sodium azide
Constituent: 99% PBS
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab190070 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/1000. Predicted molecular weight: 29 kDa.|
|IHC-P||Use a concentration of 10 µg/ml.|
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
Immunohistochemical analysis of formalin-fixed, paraffin-embedded Human skin tissue labeling Msx2/Hox8 with ab190070 at 10 µg/ml.
All lanes : Anti-Msx2/Hox8 antibody - N-terminal (ab190070) at 1/1000 dilution
Lane 1 : 293 cell lysate, non-transfected
Lane 2 : 293 cell lysate, transiently transfected with Msx2/Hox8 gene
Lysates/proteins at 2 µg per lane.
Predicted band size: 29 kDa
ab190070 has been referenced in 1 publication.
- Kero D et al. Regulation of proliferation in developing human tooth germs by MSX homeodomain proteins and cyclin-dependent kinase inhibitor p19INK4d. Organogenesis 13:141-155 (2017). PubMed: 28933666