GAMT (Guanidinoacetate N-Methyltransferase)

The identification of CA12, consistent with previous findings on its role in oncogenesis and estrogen regulation, highlights the therapeutic potential of targeting this pathway. Furthermore, the additional genes identified expand our understanding of metabolic alterations in response to estrogen signaling in breast cancer, thereby offering new avenues for mechanistic exploration and the development of potential therapeutic targets.

This study developed a prognostic model for STAD using the expression levels of MMRGs. Our findings provide insights that could inform future targeted therapeutic approaches.

This study reveals that GAMT has pro-oncogenic abilities in promoting ccRCC development and progression. GAMT exerted its non-enzymatic functions possibly by regulating the expression of p53. Fisetin, the novel GAMT inhibitor identified herein, may serve as a new antitumor drug for ccRCC treatment.

We discovered that circCGNL1 can interact with NUDT4 to enhance NUDT4-dependent HDAC4 dephosphorylation, subsequently activating HDAC4-RUNX2-GAMT-mediated apoptosis to suppress PC cell growth. These findings suggest new therapeutic targets for PC.

Experimental demyelination in mice after tamoxifen induced conditional deletion of Gamt in oligodendrocyte lineage cells resulted in delayed maturation of oligodendrocytes and myelin coverage in lesions...We found that oligodendrocytes are the main source of endogenously synthesized creatine in the adult CNS, and the loss of endogenous creatine synthesis led to delayed myelination. Our study suggests impaired cerebral creatine synthesis affects the timing of myelination and may impact brain bioenergetics.