Results 161 to 170 of about 2,429,355 (361)

Trait‐Based Life History Strategies Shape Bacterial Niche Breadth

open access: yesAdvanced Science, EarlyView.
This study investigates bacterial niche breadth through a large‐scale soil survey and over 2000 bacterial genomes. It identifies key life‐history traits—growth, competition, stress tolerance, resource acquisition, and dispersal—that correlate with niche breadth.
Ziheng Peng   +8 more
wiley   +1 more source

Bilirubin Targeting WNK1 to Alleviate NLRP3‐Mediated Neuroinflammation

open access: yesAdvanced Science, EarlyView.
At physiological concentrations, bilirubin binds to the kinase domain of WNK1, thereby augmenting its activity and facilitating the phosphorylation of downstream SPAK/OSR1. This phosphorylation inhibits KCC2 activity, leading to elevate intracellular chloride levels in neurons.
Linfei Mao   +14 more
wiley   +1 more source

Malignant Hepatoblast‐Like Cells Sustain Stemness via IGF2‐Dependent Cholesterol Accumulation in Hepatoblastoma

open access: yesAdvanced Science, EarlyView.
Hepatoblastoma, an aggressive childhood liver tumor, origins from malignant hepatoblast‐like cells. Single‐cell analysis reveals IGF2‐driven pathways promoting malignancy. Targeting these pathways offers promising treatments, with serum IGF2 as a potential diagnostic biomarker.
Miao Ding   +12 more
wiley   +1 more source

Towards an Information Theoretic Analysis of Searchable Encryption

open access: bronze, 2008
Saeed Sedghi   +3 more
openalex   +1 more source

FGF2 Mediated USP42‐PPARγ Axis Activation Ameliorates Liver Oxidative Damage and Promotes Regeneration

open access: yesAdvanced Science, EarlyView.
USP42 is identified as a novel DUB of PPARγ in hepatocytes. USP42 mediated PPARγ deubiquitylation determines its transcriptional preference on proliferative and redox balance genes. USP42 knockdown exacerbates liver damage and delays regeneration. FGF2 is the upstream signal that initiates and activates the USP42‐PPARγ axis.
Nanfei Yang   +16 more
wiley   +1 more source

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