Meiricris Tomaz da Silva

This study shows TAK1 regulates skeletal muscle mass, hypertrophy, and metabolism in both male and female mice by affecting signaling pathways and gene expression.

This study shows that inhibiting the IRE1α-XBP1 signaling pathway reduces tumor growth and promotes differentiation in rhabdomyosarcoma.

This study identifies TAK1 as a key regulator of oncogenic signaling and differentiation blockade in rhabdomyosarcoma, showing its role in promoting proliferation and inhibiting myogenic differentiation.

This study identifies molecular mechanisms of skeletal muscle wasting in pancreatic cancer cachexia using snRNA-seq and bulk RNA-seq, revealing transcription factor activity and potential therapeutic targets.

Muscle-specific XBP1 deletion or IRE1α inhibition with 4μ8C preserves muscle mass and strength in KPC pancreatic cachexia mice, curbing proteolysis, STAT3 signaling and fatty acid oxidation.

This study shows that hyperactivation of TAK1 in adult mice causes skeletal muscle pathology similar to inflammatory myopathies, while low activation improves muscle mass.

This study shows that inhibiting the TWEAK/Fn14 signaling reduces skeletal muscle wasting and tumor growth in cancer cachexia models.

This study shows that Fn14 regulates satellite cell self-renewal and expansion during skeletal muscle repair, with implications for treating muscular disorders.

This study shows that XBP1 in myofibers regulates muscle regeneration through cell-autonomous and non-autonomous mechanisms by affecting satellite cells and non-myogenic cells.