Results 71 to 80 of about 62,957 (275)
Advanced Intelligent Discovery, EarlyView.scTIGER2.0 is a deep‐learning framework that infers gene regulatory networks from single‐cell RNA sequencing data. By integrating correlation, pseudotime ordering, deep learning and bootstrap‐based significance testing, it reduces false positives and reveals directional gene interactions.
Nishi Gupta +3 more
wiley +1 more source
pFAR plasmids: New Eukaryotic Expression Vectors for Gene Therapy, devoid of Antibiotic Resistance Markers [PDF]
, 2008 Efficient production of eukaryotic expression vectors requires the selection of plasmid-containing bacteria. To avoid the risk of dissemination of antibiotic resistance markers, we developed a new system to produce a family of plasmids Free of Antibiotic
Corinne Marie +5 more
core +1 more source
Whole exome and targeted deep sequencing identify genome-wide allelic loss and frequent SETDB1 mutations in malignant pleural mesotheliomas. [PDF]
, 2016 Malignant pleural mesothelioma (MPM), a rare malignancy with a poor prognosis, is mainly caused by exposure to asbestos or other organic fibers, but the underlying genetic mechanism is not fully understood.
Fang, Li Tai +11 more
core +3 more sources
AI‐Driven Cancer Multi‐Omics: A Review From the Data Pipeline Perspective
Advanced Intelligent Discovery, EarlyView.The exponential growth of cancer multi‐omics data brings opportunities and challenges for precision oncology. This review systematically examines AI's role in addressing these challenges, covering generative models, integration architectures, Explainable AI for clinical trust, clinical applications, and key directions for clinical translation.
Shilong Liu, Shunxiang Li, Kun Qian
wiley +1 more source
European Journal of Personality, EarlyView., 2020 Abstract Vocational interests are traditionally conceived as stable preferences for different activities. However, recent theorizing suggests their intraindividual variability. This preregistered experience sampling study examined intraindividual variation in selected vocational interests states and related situation and person factors (N = 237 ...
Lena Roemer +3 more
wiley +1 more source
Nature CommunicationsNonsense mutations – the underlying cause of approximately 11% of all genetic diseases – prematurely terminate protein synthesis by mutating a sense codon to a premature stop or termination codon (PTC).
Nikhil Bharti +10 more
doaj +1 more source
Hyperphosphorylation amplifies UPF1 activity to resolve stalls in nonsense-mediated mRNA decay. [PDF]
, 2016 Many gene expression factors contain repetitive phosphorylation sites for single kinases, but the functional significance is poorly understood. Here we present evidence for hyperphosphorylation as a mechanism allowing UPF1, the central factor in nonsense-
Durand, Sébastien +2 more
core +3 more sources
Advanced Intelligent Systems, EarlyView.This article proposes NIRGB‐GS, a multimodal 3DGS variant that enables reliable 3D reconstruction and normal‐light novel‐view synthesis for extremely low‐light scenes by fusing paired near‐infrared and noisy RGB captures. High‐SNR near‐infrared modality and modality‐specific appearance encoding together resolve the issues of unstable pose/geometry ...
Chengyun Yang +3 more
wiley +1 more source
Analysis of btuB receptor function by use of nonsense suppression [PDF]
Journal of Bacteriology, 1982 Informational suppression of btuB nonsense mutants allows the study of the effect of known, single amino acid substitutions on receptor function. We found that ligand uptake is largely unaffected by such amino acid changes. The few instances in which certain substitutions destroyed sensitivity to the two lethal agents (phage BF23, colicin E3) without ...
M G, Hunter, R E, Glass
openaire +2 more sources
Therapy for Myhre Syndrome: Goals, Misconceptions, and Current Agents
American Journal of Medical Genetics Part C: Seminars in Medical Genetics, EarlyView.ABSTRACT Myhre Syndrome (MYHRS, MIM #139210) is a rare, multisystem connective tissue disorder caused by recurrent heterozygous gain‐of‐function pathogenic variants in the SMAD4 gene, a key player in TGF‐β signaling and a regulator of extracellular matrix homeostasis.
Alessandro De Falco +2 more
wiley +1 more source