The generation and characterization of true β-catenin null mutant mice conclusively demonstrate that β-catenin is dispensable for T lymphocytes and leukemia stem cells, providing clarifications on a long-standing controversy.

β-Catenin-mediated expansion of nephron progenitors is independent of direct β-catenin/chromatin engagement, while progenitor induction proceeds with a β-catenin-driven switch of repressive TCFL1/TCFL2 to activating TCF7/LEF1 factors on transcriptionally poised enhancers.

LMO2 plays an important role in the maintenance of T lymphocyte competence and survival of pre-thymic progenitors by regulating the expression of Bcl11a and Tcf7 genes.

The inclusion of a new alternatively spliced exon in Tcf7l2 can switch its function to repress transcription of Wnt target genes.

PDK1 serves as a critical role for intrinsically promoting T follicular helper cell differentiation and effector functions via controlling expression level of TCF1.

Genomic analysis of Xenopus gastrula reveal that the transcription factor Sox17 interacts with the Wnt signaling effector ß-catenin on enhancers to regulate the transcriptional program underlying endoderm germ layer formation.

Mirlet7 functions as a molecular brake of CD8⁺IL17a⁺ T cells (Tc17) inflammation and chronic obstructive pulmonary disease via direct regulation RAR-related orphan receptor gamma t (RORγt).

Normalizing Tcf4 expression during early postnatal development improves behavioral outcomes in Pitt-Hopkins syndrome (PTHS) model mice, suggesting that genetic therapies are feasible in individuals with PTHS.

Deficiency of the transcriptional repressor, Bach2, results in more mature mouse natural killer cells.

A novel population of adipocytes that play essential roles in adaptive thermogenesis via cell autonomous and non-autonomous effects and regulate systemic glucose metabolism in mice.