Results 281 to 290 of about 4,965,699 (338)

A CMTM6 Nanobody Overcomes EGFR‐TKI Resistance in Non‐Small Cell Lung Cancer

open access: yesAdvanced Science, EarlyView.
Overcoming EGFR‐TKI resistance remains a critical challenge in NSCLC treatment. This study identifies CMTM6 as a key regulator of EGFR stability and demonstrates that a novel anti‐CMTM6 nanobody disrupts the CMTM6‐EGFR interaction. Targeting CMTM6 restores EGFR degradation, suppresses tumor growth, and confers therapeutic benefit in both CDX and PDX ...
Lu Xia   +18 more
wiley   +1 more source

Inhibition of RACK1‐Mediated NLRP3 Oligomerization (Active Conformation) Ameliorates Acute Respiratory Distress Syndrome

open access: yesAdvanced Science, EarlyView.
Schematic diagram showing the potential mechanism of bigelovin on the activation of NLRP3 inflammasome Bigelovin may inhibit activated protein C kinase 1 (RACK1) by directly binding with cys168 of RACK1. Bigelovin thus prevents oligomerization of NLRP3 (NLRP3 active conformation) and subsequent assembly of NLRP3 inflammasome, blocking the activation of
Jian Cui   +17 more
wiley   +1 more source

Acod1 Promotes PAD4 Ubiquitination via UBR5 Alkylation to Modulate NETosis and Exert Protective Effects in Sepsis

open access: yesAdvanced Science, EarlyView.
In this study, Acod1 knockout in CLP mice significantly increases peripheral blood NET levels, exacerbating inflammation, organ damage, and reducing survival. Further research shows that UBR5 interacts with PAD4, a key NET formation protein. Acod1/itaconate (ITA) enhances the enzymatic activity of UBR5 by alkylating the Cys2768 site, promoting the K48 ...
Huifan Liu   +10 more
wiley   +1 more source

Cryptic Splicing of GAP43 mRNA is a Novel Hallmark of TDP‐43‐Associated ALS and AD

open access: yesAdvanced Science, EarlyView.
TDP‐43 dysfunction disrupts RNA processing, inducing cryptic exon 4a1 inclusion in GAP43 and reducing its protein levels. This aberrant splicing impairs axonal regeneration and contributes to neurodegeneration in ALS and AD. RNA‐seq of patient brains reveals GAP43 downregulation and 4a1 upregulation, identifying cryptic exon 4a1 as a potential ...
Mingming Yang   +9 more
wiley   +1 more source

Exome Sequencing Reveals the Genetic Architecture of Non‐syndromic Orofacial Clefts and Identifies BOC as a Novel Causal Gene

open access: yesAdvanced Science, EarlyView.
Nonsyndromic orofacial clefts (NSOFCs) are the most common craniofacial defects. Exome sequencing of 214 sporadic cases sheds new light on its genetic architecture and identifies many candidate pathogenic variants. Furthermore, functional studies establish BOC as a novel causal gene and reveal an unusual two‐locus model of inheritance via the epistatic
Qing He   +16 more
wiley   +1 more source

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