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Function: require_once
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Filename: controllers/Detail.php
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Function: _error_handler
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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Function: _error_handler
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Function: require_once
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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Function: _error_handler
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Filename: models/Detail_model.php
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Function: strpos
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Function: insertAPISummary
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Filename: helpers/my_audit_helper.php
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File: /var/www/html/application/helpers/my_audit_helper.php
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Function: str_replace
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Function: formatAIDetailSummary
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Ageing can be defined as the gradual deterioration of physiological functions, increasing the incidence of age-related disorders and the probability of death. Therefore, the term ageing not only reflects the lifespan of an organism but also refers to progressive functional impairment and disease. The nutrient-sensing kinase mTOR (mammalian target of rapamycin) is a major determinant of ageing. mTOR promotes cell growth and controls central metabolic pathways including protein biosynthesis, autophagy and glucose and lipid homoeostasis. The concept that mTOR has a crucial role in ageing is supported by numerous reports on the lifespan-prolonging effects of the mTOR inhibitor rapamycin in invertebrate and vertebrate model organisms. Dietary restriction increases lifespan and delays ageing phenotypes as well and mTOR has been assigned a major role in this process. This may suggest a causal relationship between the lifespan of an organism and its metabolic phenotype. More than 25 years after mTOR's discovery, a wealth of metabolic and ageing-related effects have been reported. In this review, we cover the current view on the contribution of the different elements of the mTOR signalling network to lifespan and age-related metabolic impairment. We specifically focus on distinct roles of isoforms and splice variants across the mTOR network. The comprehensive analysis of mouse knockout studies targeting these variants does not support a tight correlation between lifespan prolongation and improved metabolic phenotypes and questions the strict causal relationship between them.
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http://dx.doi.org/10.1042/EBC20160086 | DOI Listing |
Mol Ther Oncol
December 2024
Center for Childhood Cancer Research, Abigail Wexner Research Institute at Nationwide Children's Hospital, Columbus, OH 43215, USA.
Patients with osteosarcoma (OS), a debilitating pediatric bone malignancy, have limited treatment options to combat aggressive disease. OS thrives on insulin growth factor (IGF)-mediated signaling that can facilitate cell proliferation. Previous efforts to target IGF-1R signaling were mostly unsuccessful, likely due to compensatory signaling through alternative splicing of the insulin receptor () to the proliferative isoform.
View Article and Find Full Text PDFInt J Biol Macromol
December 2024
Integrative Science Center of Germplasm Creation in Western China (CHONGQING) Science City, Biological Science Research Center, Southwest University, Chongqing 400715, China; Chongqing Engineering and Technology Research Center for Novel Silk Materials, Southwest University, Chongqing 400715, China. Electronic address:
The abnormal development of urate granules in silkworm larvae leads to translucent mutants with a distinct transparent phenotype. Studies on such mutants are expected to enhance current understanding of uric acid metabolism. The hoarfrost translucent (oh) mutant exhibits a mottled, translucent larval integument due to the presence of smaller and irregularly shaped urate granules compared to wild-type individuals.
View Article and Find Full Text PDFMol Biol Cell
December 2024
i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal.
The microtubule motor cytoplasmic dynein-1 transports and positions various organelles, but the molecular basis of this functional diversity is not fully understood. Cargo adaptors of the Hook protein family recruit dynein to early endosomes (EE) in fungi and human cells by forming the FTS-Hook-FHIP (FHF) complex. By contrast, the Hook homolog ZYG-12 recruits dynein to the nuclear envelope (NE) in the meiotic gonad and mitotic early embryo by forming a Linker of Nucleoskeleton and Cytoskeleton (LINC) complex.
View Article and Find Full Text PDFAnn Med
December 2025
Department of Breast Surgery, Second Affiliated Hospital and Cancer Institute (Provincial Key Laboratory of Tumor Microenvironment and Immunotherapy, Key Laboratory of Cancer Prevention & Intervention, National Ministry of Education), Zhejiang University School of Medicine, Hangzhou, China.
Background: Quaking (QKI) is a member of the signal transduction and activators of RNA (STAR) family, performing a crucial multifunctional regulatory role in alternative splicing, mRNA precursor processing, mRNA transport and localization, mRNA stabilization, and translation during tumour progression. Abnormal QKI expression or fusion mutations lead to aberrant RNA and protein expression, thereby promoting tumour progression. However, in many types of tumour, QKI played a role as tumour suppressor, the regulatory role of QKI in tumour progression remains ambiguous.
View Article and Find Full Text PDFOrphanet J Rare Dis
December 2024
Department of Health Sciences, Università degli Studi di Milano, Milan, Italy.
Background: the protein phosphatase 3 catalytic subunit alpha (PPP3CA) gene encodes for the alpha isoform of the calcineurin catalytic subunit, which controls the phosphorylation status of many targets. Currently, 23 pathogenic variants of PPP3CA are known, with clinical manifestations varying by mutation type and domain.
Results: through whole exome sequencing, we found two de novo variants in PPP3CA: a frameshift variant predicted leading to a truncated protein in Pt.
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