Micall2-flox Mouse

Micall2, also known as molecule interacting with CasL-like protein 2, is believed to regulate cytoskeleton dynamics, tight junction formation, and neurite outgrowth. It has been associated with multiple biological processes and diseases, and is involved in pathways such as the Wnt/β -catenin signaling pathway [2,3]. Genetic models are valuable for studying its functions.

In clear cell renal cell carcinoma (ccRCC), Micall2 was highly expressed in cancer tissues and cell lines compared to normal tissues. Overexpression promoted, while gene silencing inhibited, the proliferation, migration, and invasion of ccRCC cells, suggesting it contributes to ccRCC malignancy [1].

In colorectal cancer, its overexpression was correlated with poor prognosis, and it enhanced cell growth and migration via the Wnt/β -catenin pathway. Ubiquitin E3 ligase TRIM21 mediated its ubiquitination and degradation [2].

In pulmonary fibrosis, knockdown of Micall2 in mice and cells restrained the epithelial-mesenchymal transition (EMT) process by impeding β -catenin nuclear translocation [3].

In ovarian cancer, bioinformatics analysis showed its high expression in advanced-stage tissues, and it participated in immune infiltration and invasion, preventing EGFR degradation in a Rac1-dependent manner [4].

In Ashidan yaks, copy number variations in the Micall2 gene were associated with growth traits [5].

In children with attention deficit hyperactivity disorder (ADHD), a locus regulating Micall2 expression was associated with executive inhibition, and reducing the expression of its homologous gene in zebrafish induced hyperactive-impulsive-like behavior [6].

In conclusion, Micall2 plays crucial roles in various biological processes and diseases. Studies using gene-manipulation models, such as gene knockdown in mice and cells, have revealed its pro-tumorigenic role in cancers like ccRCC, colorectal cancer, and ovarian cancer. It also has implications in pulmonary fibrosis, animal growth traits, and ADHD. These findings provide valuable insights into understanding disease mechanisms and potential therapeutic targets related to Micall2.