K. E. Leon

NF-κB inhibitor alpha has a cross-variant role during SARS-CoV-2 infection in ACE2-overexpressing human airway organoids

The paper uses ACE2-overexpressing airway organoids to show NF-κB inhibitor alpha is upregulated during SARS-CoV-2 infection and its reduced function increases viral infection.

Zika Virus Infection Prevents Host mRNA Nuclear Export by Disrupting UPF1 Function

This study shows ZIKV infection disrupts UPF1 function, leading to nuclear mRNA accumulation and impaired neural progenitor cell function.

DOT1L modulates the senescence-associated secretory phenotype through epigenetic regulation of IL1A

This study shows that DOT1L regulates the senescence-associated secretory phenotype (SASP) through epigenetic control of IL1A expression in oncogene-induced senescence.

Suppression of p16 alleviates the senescence-associated secretory phenotype

This study shows that reducing p16 expression lowers SASP factor and cytokine levels in senescent cells without affecting senescence markers.

ATM Inhibition Synergizes with Fenofibrate in High Grade Serous Ovarian Cancer Cells

This study shows that combining ATM inhibitors with fenofibrate improves treatment in high-grade serous ovarian cancer cells by inducing senescence.

ATM inhibition drives metabolic adaptation via induction of macropinocytosis

This study shows that ATM inhibition promotes cancer cell survival by increasing macropinocytosis, which can be suppressed by BCAA supplementation.

Suppression of p16 increases nucleotide synthesis via mTORC1

This study shows that p16 suppression increases nucleotide synthesis through mTORC1 activation, promoting tumorigenesis by bypassing senescence.

Targeting IDH1 as a pro-senescent therapy in high-grade serous ovarian cancer

This study identifies IDH1 as a therapeutic target in HGSC by showing its role in promoting metabolic adaptation and epigenetic repression, leading to senescence when inhibited.

The cellular NMD pathway restricts Zika virus infection and is targeted by the viral capsid protein

This study shows that ZIKV infection disrupts the NMD pathway by interacting with UPF1 via its capsid protein, enhancing viral infection and contributing to neuropathology.