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Trisomy 21, the genetic cause of Down syndrome, produces elevated centrosome protein levels reducing intracellular trafficking to and from the centrosome thereby delaying primary ciliogenesis, ciliary signaling, and mouse cerebellar development.

In the absence of ROCK1 activation by caspases, apoptotic cells don’t undergo typical morphological changes, leading to sterile inflammation in the liver that increases tissue damage and suppresses tumor formation.

Macrophage production of MT1-MMP upon MI contributes to adverse cardiac remodeling and worsened function by promoting EndMT via TGFB, suggesting MT1-MMP inhibition as a therapeutic option for patients with MI.

Virus infection in mosquitoes initiates a highly discriminatory process in which fragments of viral RNA are reverse transcribed to create DNA copies that serve as templates of small antiviral RNAs.

MAD1 and TPRN were identified as novel potential therapeutic targets of lung adenocarcinoma in female never-smokers from the Xuanwei area.

Synthetic biology experiments show that MYC is a general transcription amplifier acting at two or more sites in the transcription-cycle and that MYC-turnover contributes to its activity.

Network propagation connects TWIST1 with epigenetic regulators CHD7, CHD8, and WHSC1, which collectively promote the bias toward neural crest while suppressing neural stem cell programmes, and subsequently enhance ectomesenchyme potential.

Erastin and sorafenib inhibit system x_c^- and induce ER stress, suggesting these may be useful tools for probing the functions of system x_c^- and its role in inducing ER stress and ferroptosis.

Enriching amphibian, Xenopus laevis, cutaneous mast cells confers protection against Batrachochytrium dendrobatidis chytrid fungus infections.