Adaptor for 16 mm tube
- Known as:
- Adaptor 16 millimeter tube
- Catalog number:
- CSL-TS-B16
- Category:
- -
- Supplier:
- Cleaver
- Gene target:
- Adaptor for 16 tube
Related genes to: Adaptor for 16 mm tube
- Gene:
- TSC2 NIH gene
- Name:
- TSC complex subunit 2
- Previous symbol:
- TSC4
- Synonyms:
- tuberin, LAM, PPP1R160
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-25
- Date modifiied:
- 2019-04-23
Related products to: Adaptor for 16 mm tube
Related articles to: Adaptor for 16 mm tube
- The natural history of pancreatic neuroendocrine tumors (NETs) can span decades of slow progression, but it is unpredictable, with a more aggressive course also being common. The two clinical biomarkers currently used to define the grade of a tumor, the Ki67 index and the mitotic index, are not able to fully capture the course of individual patients. This creates an unmet need to discover better prognostic biomarkers to inform therapeutic decisions, as well as therapies with overall survival benefit. Two genomic series of pancreatic NETs were examined to discover sub-sets with divergent characteristics. Primary data were downloaded from the cBioportal cancer genomics portal and analyzed at the individual sample level. Pancreatic NET patients without // mutations were younger than NET patients with any of these mutations. Pancreatic NETs had consistently low tumor mutation burden but were heterogeneous in their Fraction Genome Altered (FGA), a metric of chromosomal instability (CIN), with one group presenting high FGA and another possessing low to intermediate FGA. FGA did not correlate with Ki67, but high FGA was most prevalent in cases with mutations in and or . mutations were significantly more prevalent in the group with high FGA. - Source: PubMed
Publication date: 2026/09/08
Voutsadakis Ioannis A - Tuberous sclerosis complex (TSC) is a genetic neurodevelopmental disorder characterized by focal brain malformations called cortical tubers, which are associated with severe, intractable epilepsy. Tubers are thought to result from somatic second-hit mutations that disrupt the TSC1 or TSC2 genes in neural progenitor cells, driving hyperactive mTORC1 signalling. Glial abnormalities are commonly observed in tubers; however, whether glia actively cause disease or merely result from chronic seizure activity has remained unclear. To address this question, we used human brain organoid models to track the developmental fate of mutated progenitor cells in the absence of seizures. Here we show, using single-cell transcriptomics and cyclic immunostaining across human brain organoids and resected tuber tissue from patients, that loss of TSC2 biases neural progenitors to differentiate into enlarged, pro-inflammatory reactive astrocytes in a cell autonomous manner. These mutant astrocytes show downregulated glutamate transporter expression, increased inflammatory cytokine secretion and elevated expression of neurodegenerative disease risk genes such as APOE and CLU. Our findings demonstrate that reactive astrocytes emerge as a primary consequence of TSC2 loss. These results implicate glial dysfunction as a driver of TSC pathogenesis and highlight reactive astrocytes as potential therapeutic targets for TSC-related neuropathology. - Source: PubMed
Publication date: 2026/09/23
Li Thomas LBlair John DYoo TaesunGrant Gerald AHockemeyer DirkPorter Brenda EBateup Helen S - Neurodevelopmental disorders (NDDs) are characterized by a spectrum of cognitive, behavioral, and affective morbidities, reflecting underlying disruptions in neural circuit development. Emerging evidence implicates translational dysregulation of synaptic proteins as a central mechanistic driver of these disordered phenotypes. Translational dysregulation entails atypical mechanisms of impaired initiation, elongation, and mRNA targeting, causing imbalanced protein synthesis. In NDDs specifically, translation of synaptic proteins is perturbed across developing neurons. Tuberous Sclerosis Complex (TSC) and Fragile X Syndrome (FXS) are notable monogenic NDDs, in which mutations in regulatory genes (Tsc1/Tsc2 in TSC, Fmr1 in FXS) disrupt signaling pathways that converge on mTORC1, PERK, and ERK/MAPK proteins, and result in excessive or insufficient translation of key synaptic proteins. These translational imbalances eventually compromise synapse formation, dendritic spine maturation, and neuronal network connectivity, contributing to deficits in learning, memory, social behavior, and emotional regulation. This review highlights the molecular mechanisms by which aberrant protein synthesis contributes to the cognitive and behavioral manifestations of TSC and FXS. Importantly, we also highlight cell-type-specific mechanisms, illustrating how translational dysregulation differentially impacts distinct neuronal and glial populations to shape behavioral and cognitive outcomes. Understanding the links between translational control and neurodevelopmental outcomes provides critical insights into the pathophysiology of these disorders and informs the development of targeted therapeutic interventions aimed at restoring synaptic protein homeostasis. - Source: PubMed
Publication date: 2026/09/19
Lawal SaheedMujtaba MonizaShrestha Prerana - Tryptophan is an essential dietary amino acid and the sole precursor of serotonin (5-HT), a neurotransmitter that plays a key role in cognition, mood regulation, and sensory processing. Because central serotonin synthesis depends on dietary tryptophan availability, nutritional modulation of tryptophan intake has emerged as a potential strategy to influence brain function and behavior. Disruptions in tryptophan metabolism and serotonergic signaling have been implicated in autism spectrum disorder (ASD), particularly in Tuberous Sclerosis Complex (TSC), a neurogenetic condition frequently associated with ASD. In this study, we investigated whether dietary tryptophan supplementation could modulate brain tryptophan metabolism and improve ASD-related behaviors in the mouse model. For that, behavioral tests were performed together with magnetic resonance spetrosocopy (H-MRS) and high-performance liquid chromatography (HPLC). Behavioral analysis revealed sex-specific improvements following supplementation, including enhanced sociability in females, restoration of social novelty preference in males, and reduced anxiety-like behavior accompanied by increased exploratory activity across groups. These behavioral changes were associated with increased cortical tryptophan levels, as determined by high-performance liquid chromatography. However, no significant alterations in cortical excitation/inhibition balance were detected using proton magnetic resonance spectroscopy. Together, these findings demonstrate that dietary tryptophan supplementation enhances cortical tryptophan availability and ameliorates ASD-like behavioral phenotypes in mice. Our results highlight the potential of nutritional modulation of tryptophan intake as a non-invasive strategy to influence serotonergic pathways and behavioral outcomes, supporting the development of precision nutrition approaches for neurodevelopmental disorders. - Source: PubMed
Publication date: 2026/09/18
Lapo Pais MarianaFonseca CarlaMartins JoãoFortuna AnaCastelo-Branco MiguelGonçalves Joana - To explore the molecular mechanism of tuberous sclerosis type 2 caused by TSC2 synonymous mutations affecting normal splicing of precursor mRNA. - Source: PubMed
Publication date: 2026/06/25
Zhang ChuanjieLi SijunLeng RunlingDeng MinYang Guohua