Anti-Msx2/Hox8 antibody - N-terminal (ab190070)

Overview

  • Product name
    Anti-Msx2/Hox8 antibody - N-terminal
    See all Msx2/Hox8 primary antibodies
  • Description
    Rabbit polyclonal to Msx2/Hox8 - N-terminal
  • Host species
    Rabbit
  • Tested applications
    Suitable for: WB, IHC-Pmore details
  • Species reactivity
    Reacts with: Human
  • Immunogen

    Synthetic peptide corresponding to Human Msx2/Hox8 (N terminal) conjugated to Keyhole Limpet Haemocyanin (KLH). NP_002440.2.
    Database link: P35548

  • Positive control
    • Human skin tissue; 293 cell lysates transiently transfected with the Msx2/Hox8 gene.

Properties

Applications

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.

Application Abreviews Notes
WB 1/1000. Predicted molecular weight: 29 kDa.
IHC-P Use a concentration of 10 µg/ml.

Target

  • Function
    Acts 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 disease
    Defects 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 similarities
    Belongs to the Msh homeobox family.
    Contains 1 homeobox DNA-binding domain.
  • Cellular localization
    Nucleus.
  • Information by UniProt
  • Database links
  • Alternative names
    • CRS 2 antibody
    • CRS2 antibody
    • FPP antibody
    • Homeo box msh like 2 antibody
    • Homeobox protein Hox-8 antibody
    • Homeobox protein MSX 2 antibody
    • Homeobox protein MSX-2 antibody
    • Homeobox protein MSX2 antibody
    • Hox 8 antibody
    • Hox8 antibody
    • MSH antibody
    • Msh homeo box 2 antibody
    • Msh homeo box homolog antibody
    • Msh homeo box homolog 2 antibody
    • Msh homeobox 2 antibody
    • Msh homeobox homolog 2 antibody
    • Msx 2 antibody
    • MSX2 antibody
    • MSX2_HUMAN antibody
    • Parietal foramina 1 antibody
    • PFM 1 antibody
    • PFM antibody
    • PFM1 antibody
    see all

Images

  • 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

References

ab190070 has not yet been referenced specifically in any publications.

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Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"

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