Rbm28, also known as RNA-binding motif protein 28, is a nucleolar component of spliceosomal small nuclear ribonucleoproteins. It is involved in the nucleolar stress response, and its yeast ortholog Nop4p is known to regulate ribosome biogenesis [4,8]. Rbm28 is also associated with pathways related to tumor suppression, hair follicle growth, and angiogenesis [1,3,6].

In cancer, Rbm28 is frequently overexpressed, promoting cancer cell survival and growth by inhibiting the transcriptional activity of the tumor suppressor p53. For example, upon treatment with chemotherapeutic drugs, Rbm28 translocates from the nucleolus to the nucleoplasm, likely mediated by phosphorylation at Ser122 by Chk1/2 [1]. In colorectal cancer, USP36 stabilizes Rbm28 via deubiquitination, which in turn suppresses p53 transcriptional activity [2]. In hepatocellular carcinoma, increased Rbm28 expression enhances angiogenesis by improving STAT3 translation [6]. In ANE syndrome, a rare inherited disorder, decreased expression of Rbm28 leads to alopecia, neurological defects, and endocrinopathy. In human hair follicle organ cultures, down-regulation of Rbm28 results in catagen induction and hair growth arrest, and Rbm28 is shown to regulate miR-203 and p63 which are important for hair morphogenesis [3,5,7,8].

In conclusion, Rbm28 plays crucial roles in multiple biological processes. Its overexpression in cancers promotes tumor progression, while its deficiency causes ANE syndrome. Studies on Rbm28, including those using potential genetic models like KO or CKO mouse models (although not directly mentioned in the given references), could further clarify its functions and potentially lead to new therapeutic strategies for related diseases.