High impact information on Itm2a

• The mouse E25 gene locus (Itm2) was mapped to the X chromosome [1].
• MMP-13 expression was restricted to chondrocytes of the lower zone of hypertrophic cartilage also expressing collagen type X. In osteoblasts involved in endochondral and intramembranous ossification Itm2a was not present [2].
• In areas undergoing endochondral ossification Itm2a expression was found in chondrocytes of the resting and the proliferating zones [2].
• During embryonic development expression of Itm2a and ALP was detectable at midgestation (11.5 days postcoitum [dpc]) and increased up to 16.5 dpc [2].
• The Itm2a gene contains six exons and five introns [3].

Biological context of Itm2a

• Itm2a cDNA was originally isolated from a cDNA library of organ cultures from prenatal mouse mandibular condyles, by subtractive hybridization and differential screening [3].
• The Itm2a gene was isolated from a BALB/c liver genomic library [3].
• Itm2a was mapped to mouse chromosome position XA2-XA3 by fluorescent in situ hybridization (FISH) analysis [3].
• Taken together, our observation supports the involvement of Itm2a in the early stages of chondrogenesis in vitro [4].

Anatomical context of Itm2a

• Targeting via the anti-fibronectin antibody and anti-endothelial antiserum provided maximal quantitative binding of glucose oxidase to endothelial cells, while the conjugates with MoAb E25 and MoAb E78 monoclonal antibodies provided less effective binding [5].

Associations of Itm2a with chemical compounds

• Though the quantitative binding of MoAb E25-conjugated glucose oxidase was minimal comparing to other conjugates, targeting via MoAb E25 produced the maximal cytotoxic effect as well as targeting via polyclonal antiserum [5].

Regulatory relationships of Itm2a

• These results demonstrate that overexpression of Itm2a in C2C12 enhances myogenic differentiation in vitro [6].

References