Metastasis-associated protein 1 (MTA1) regulates the catecholamine production homeostasis via transcriptional repression of aromatic l-amino acid decarboxylase (Aadc) in the interstitial cells of Cajal of mouse prostate.
MTA1 participates in the formation of pulmonary capillaries via stabilization of HIF-1alpha. This finding sheds new light on the function of MTA1 in lung development.
Findings illustrate how cancer cells utilize a chromatin remodeling factor to engage a core survival pathway to support its cancerous phenotypes and reveal new facets of MTA1-SGK1 axis by a physiologic signal in cancer progression.
Inhibition of MTA1 expression by in vivo siRNA treatment exacerbated the pathology of LPS-induced acute lung injury by selectively promoting the expression of NF-kappaB-regulated inflammatory cytokines.
the augmentation of endogenous MTA1 expression during neuronal ischemic injury acts additionally to an endocrinous cascade orchestrating intimate interactions between ERalpha and BCL2 pathways.
this study reports the potential signaling events related to up-regulation of metastasis associated protein 1 (Mta1) a master chromatin modifier during mono-(2-ethylhexyl) phthalate (MEHP)-induced Sertoli cells injury.
Data suggest that nuclear metastasis-associated protein 1 (MTA1) is a good marker for cancer differentiation diagnosis and a potential target for the treatment of cancers.
the MTA1/NFkappaB/FasL circuit may serve as an important defensive/repairing mechanism to help to control the germ cell quality after Sertoli cell injury.
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