Check the content of the review Id1, short for Inhibitor of DNA binding 1, is a key transcriptional regulator. It is involved in multiple biological processes such as cell cycle regulation, cell differentiation, and maintaining stem-cell-like properties. Id1 is associated with numerous signaling pathways, including EMT-related proteins, K-Ras, EGFR, BMP, PI3K/Akt, WNT, SHH, c-Myc, STAT3, RK1/2 MAPK/Egr1, and TGF-β pathways [2].

Knocking out Id1 in mesenchymal cells significantly suppresses the proliferation of cocultured AML cells, and loss of Id1 in the BMM impairs AML progression in AML mouse models. The mechanism involves a decrease in SP1 protein levels in mesenchymal cells due to Id1 deficiency, which is related to the interaction between ID1 and RNF4, an E3 ubiquitin ligase. The target of Sp1, Angptl7, is the primary differentially expressed protein factor in Id1-deficient BM supernatant fluid to regulate AML progression in mice [1]. In Th9 cell differentiation, Id1-deficient naïve CD4 T cells fail to differentiate into Th9 cells, as Id1 is induced by IL-4 and TGF-β and inhibits Tcf3 and Tcf4, which bind to the promoter region of the Il9 gene to suppress its expression [3].

In conclusion, Id1 is crucial in regulating cell-related biological processes and plays important roles in diseases like AML and in Th9 cell-related immune responses. The use of gene knockout mouse models has significantly enhanced our understanding of Id1's functions in these specific biological processes and disease conditions, providing potential targets for therapeutic strategies.