Редактирование: MN1

Transcriptional activator MN1 (Probable tumor suppressor protein MN1)

==Publications==

{{medline-entry
|title=Targeted disruption of the Mn1 oncogene results in severe defects in development of membranous bones of the cranial skeleton.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/15870292
|abstract=Fusion of the [[MN1]] gene to TEL (ETV6) results in myeloid leukemia. The fusion protein combines the transcription activating domain of [[MN1]] and the DNA binding domain of TEL and is thought to act as a deranged transcription factor. In addition, disruption of the large first exon of the [[MN1]] gene is thought to inactivate [[MN1]] function in a meningioma. To further investigate the role of [[MN1]] in cancer, we generated Mn1 knockout mice. Mn1( /-) animals were followed for 30 months, but they had no higher incidence of tumor formation than wild-type littermates. Mn1 null mice, however, were found to die at birth or shortly thereafter as the result of a cleft palate. Investigation of newborn or embryonic day 15.5 (E15.5) to E17.5 null mice revealed that the development of several bones in the skull was abnormal. The affected bones are almost exclusively formed by intramembranous ossification. They are either completely agenic at birth (alisphenoid and squamosal bones and vomer), hypoplastic, deformed (basisphenoid, pterygoid, and presphenoid), or substantially thinner (frontal, parietal, and interparietal bones). In heterozygous mice hypoplastic membranous bones and incomplete penetrance of the cleft palate were observed. We conclude that Mn1 is an important factor in development of membranous bones.
|mesh-terms=* Aging
* Animals
* Animals, Newborn
* Cleft Palate
* Gene Deletion
* Head
* Heterozygote
* Homozygote
* Longevity
* Mice
* Mice, Knockout
* Oncogene Proteins
* Organ Specificity
* Skull
* Survival Analysis
* Trans-Activators
* Tumor Suppressor Proteins

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1087735
}}