Ezh2 and Arid1a oppose each other to control expression of Cdkn2a to coordinate tooth furcation development and ultimately determine the number of roots in mouse molars.

ARID1A deficiency in SWI/SNF complex promotes pancreatic tumor development by upregulating ALDH protein levels to effectively reduce cellular reactive oxygen species levels, leading to the significant attenuation of oncogenic KRAS-induced senescence.

ARID1A, a subunit of the SWI/SNF chromatin remodeling complex, and its homolog ARID1B function to maintain chromatin accessibility and active histone modifications at enhancers.

Mirroring human patients with ARID1B mutations, Arid1b haploinsufficient mice exhibited numerous neuropsychiatric defects and revealed IGF1 deficiency related growth impairment that could be ameliorated with growth hormone supplementation.

Pain sensation induces relapse in a mouse model of multiple sclerosis via a sensory-sympathetic signaling pathway.

An interaction between the ion channel ASIC1a and the protein RIP1 is responsible for neuronal death caused by tissue acidosis.

Arid3a, a component of H3K9 me3 demethylases, regulates regeneration of the proximal nephric tubule through the evolutionarily conserved regeneration signal-response enhancer.

Arid1a loss in the pancreas enables an irreversible reprogramming of cell fate that is dependent on both cellular and genetic context.

A link between chronic stress and organ dysfunction is explained by the gateway reflex, in which brain micro-inflammation at specific vessels establishes a new neural pathway to induce fatal organ failure particularly in gastrointestine and heart.

A chromatin remodeling factor cooperates with Wnt signaling pathway to transcribe erythropoietin in the adult liver, inducing its secretion and a dramatic erythropoiesis in the spleen.