1.5 ml microcentrifuge tube, clear, graduated
- Known as:
- 1.5 milliliter microcentrifuge tube, clear, graduated
- Catalog number:
- KG2211
- Product Quantity:
- 500 pcs/bag, 10 bag/cs
- Category:
- -
- Supplier:
- Kirgen Bioscience
- Gene target:
- 1.5 microcentrifuge tube clear graduated
Related genes to: 1.5 ml microcentrifuge tube, clear, graduated
- 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: 1.5 ml microcentrifuge tube, clear, graduated
Related articles to: 1.5 ml microcentrifuge tube, clear, graduated
- Activation of the mechanistic target of rapamycin (mTOR) complex1 (mTORC1) promotes muscle protein synthesis, mass, and function. Muscle mTORC1 can be activated by feeding and contraction. Here, muscle mTORC1 signaling, protein synthesis, mass, and function are characterized in a genetic mouse model that separates these two major modes of muscle mTORC1 regulation. AKT signaling is required for feeding-induced muscle mTORC1 signaling and protein synthesis, and mice expressing a mutant of tuberous sclerosis complex 2 (TSC2) that cannot be phosphorylated by AKT specifically in skeletal muscle (SkM-TSC2-5A) attenuate these effects of feeding. Despite this loss of postprandial protein synthesis, SkM-TSC2-5A mice have similar muscle and myofiber size compared to SkM-TSC2-WT mice. SkM-TSC2-5A mice maintain normal muscle mTORC1 activation in response to contraction and exhibit no differences in atrophy-related gene expression or ribosomal content. SkM-TSC2-5A mice exhibit improved maximal endurance capacity without changes in muscle contractile function. This phenotype occurs without alterations in muscle glycogen content or myofiber type but does coincide with a modest increase in muscle mitochondrial content. Therefore, AKT-mediated phosphorylation of TSC2 is required for postprandial mTORC1 activation and the induction of protein synthesis; however, these are dispensable for the development and maintenance of muscle mass in sedentary mice. - Source: PubMed
Publication date: 2026/09/10
Lapp Samuel CKalafut Krystle CCissé Madi YTighanimine KhaledRosenthal Dean MDoxsey WillHui ShengInouye Karen EMorrow Claire ECormerais YannManning Brendan D - Acquired resistance to mTOR inhibition remains a major challenge in TSC2-mutant metastatic epithelioid angiomyolipoma (EAML). We report a 30-year-old woman with metastatic EAML harboring biallelic TSC2 mutations who achieved a complete response to everolimus but developed disease progression after 16 months. Tumor rebiopsy revealed persistent TSC2 mutations and acquired CDKN2A/B deletion, accompanied by increased Ki-67 and emergence of TFE-3 immunoreactivity and focal S-100 positivity. These findings suggest a potential association between CDKN2A/B loss and aggressive tumor behavior after mTOR inhibition, although causality remains unproven. CDK4/6-targeted strategies may warrant further investigation in this context. - Source: PubMed
Publication date: 2026/08/25
He ShuaiYang JingYang JiguangLi ChunxiaShen JuanYe XiaolongLiu ZupingShen WenhaoZheng JunWang Yongquan - Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by altered synaptic connectivity and network organization, resulting in profound impairments in social communication and interaction. Transcranial direct current stimulation (tDCS) represents a promising approach to modulate maladaptive plasticity associated with ASD; however, mechanistic evidence from preclinical models remains limited. Here, we investigated whether repeated anodal tDCS targeting the medial prefrontal cortex modulates ASD-relevant social behavioral deficits in a rodent model. Male Tsc2 rats with induced developmental status epilepticus (DSE) and wild-type (WT) littermate controls received repeated anodal tDCS (200 μA for 20 min, twice daily) for 12 consecutive days. Social behavior profiles were evaluated at baseline and at 2- and 5 weeks following treatment. In addition, postmortem analyses investigated neuroplasticity-related markers and monoaminergic neurotransmitter levels. tDCS selectively modulated social behavioral deficits in Tsc2 DSE rats. Specifically, tDCS in Tsc2 DSE rats caused a sustained reduction in social avoidance and transient improvements in social exploration, while social approach behavior improved but did not return to WT levels, and social recognition impairments remained unaffected. In addition, tDCS restored abnormal serotonin levels in brain regions involved in social behavior, suggesting a potential contribution of serotonergic mechanisms to the observed behavioral effects. Our results demonstrate that improvements in some domains of ASD-relevant social deficits following tDCS persist for weeks beyond the stimulation period, possibly through neuroplastic modulation of serotonergic neurotransmission. Together, these results provide mechanistic insights into how noninvasive brain stimulation may modulate specific components of social dysfunction and highlight the importance of considering the multidimensional nature of ASD-related behaviors when evaluating therapeutic interventions. - Source: PubMed
Publication date: 2026/09/08
Ramme AntoniaWinter RebeccaJarzebska NataliaÖgel FatihRichter Marten JulianVojtechova IvetaWinter ChristinePetrasek TomasWaltereit RobertBernhardt Nadine - Fragile X syndrome (FXS) and tuberous sclerosis complex (TSC) are common monogenic causes of autism spectrum disorder (ASD). FXS arises from FMR1 silencing, while TSC results from mutations in TSC1 or TSC2, both converging on dysregulated ERK and mTORC1 signaling. Animal knockout models suggest opposing effects on synaptic plasticity, with reciprocal compensation in double knockouts (dKO). However, clinical case with dual mutations shows severe neurodevelopmental deficits; here, we explored a human cellular model to dissect the shared and divergent mechanisms. We generated isogenic human pluripotent stem cell (hPSC)-derived models of FMR1KO, TSC2KO, and FMR1/TSC2 dKO neurons. Neuronal transcriptomes were profiled by RNA-seq, integrating ERK, mTOR, FMRP targets, and ASD risk genes. Validation via qPCR of key genes, protein synthesis, proliferation assays, and microelectrode array was performed. The FMR1/TSC2 dKO neural progenitor cells (NPCs) demonstrated high DNA damage response but normalized proliferation. Convergent transcriptomic pathways across FMR1KO, TSC2KO, and dKO neurons included upregulated extracellular matrix and stress responses, and downregulated synaptic and neurotransmission-related pathways. TSC2KO and dKO neurons showed greater similarity transcriptionally and functionally. Translational pathways and global protein synthesis were oppositely regulated in TSC2KO and dKO versus FMR1KO neurons. The dKO neurons showed hyperexcitable network activity, mTOR hyperactivation, with distinct dysregulated FMRP targets and ASD risk gene expression. Unlike mouse models, FMR1/TSC2 dKO hPSC-derived neurons did not show rescue of synaptic gene expression. Rather, dKO neurons predominantly resembled TSC2KO neurons with translational, synaptic, and neurotransmission abnormalities. These findings highlight complex interplay between FMRP and TSC, providing a foundation for future studies of ASD-relevant mechanisms. - Source: PubMed
Publication date: 2026/09/08
Utami Kagistia HanaYusof Nur Amirah Binte MuhammedRamaswamy YazhiniTay Stacey Kiat HongAishworiya RamkumarTham NevinLangley Sarah RPouladi Mahmoud AHan Velda X - To report the first detailed description of the radiological features of tuberous sclerosis complex 2/polycystic kidney disease 1 (TSC2/PKD1) contiguous gene deletion syndrome (CGS), a rare and poorly reported or described syndrome. - Source: PubMed
Publication date: 2026/09/04
Bitton JulienBoudhabhay IdrisDariane CharlesEssig MarieTourret JeromeAudrezet Marie-PierreHummel AurélieKnebelmann BertrandCorreas Jean-MichelHélénon OlivierBodard Sylvain