WB | 咨询技术 | Human,Mouse,Rat |
IF | 咨询技术 | Human,Mouse,Rat |
IHC | 咨询技术 | Human,Mouse,Rat |
ICC | 技术咨询 | Human,Mouse,Rat |
FCM | 咨询技术 | Human,Mouse,Rat |
Elisa | 咨询技术 | Human,Mouse,Rat |
Aliases | Hamartin, Tuberous sclerosis 1 protein, TSC1, KIAA0243, TSC |
Entrez GeneID | 7248 |
WB Predicted band size | 129.8kDa |
Host/Isotype | Rabbit IgG |
Antibody Type | Primary antibody |
Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
Species Reactivity | Human |
Immunogen | This TSC1 Antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding S505 of human TSC1. |
Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是3篇涉及TSC1磷酸化(含S505位点)的文献摘要及作者信息:
1. **文献名称**:*mTOR signaling in growth control and disease*
**作者**:Laplante M, Sabatini DM
**摘要**:该综述系统总结了mTOR信号通路的调控机制,指出TSC1/TSC2复合体作为mTORC1上游抑制因子,其磷酸化状态(如TSC1的S505位点)通过响应生长因子和能量状态调控细胞增殖与代谢。
2. **文献名称**:*Phosphorylation of TSC1 by AMPK regulates mTORC1 signaling*
**作者**:Inoki K, et al.
**摘要**:研究发现AMPK通过磷酸化TSC1(包括S505位点)增强TSC复合体活性,从而抑制mTORC1.揭示能量应激条件下细胞生长调控的分子机制。
3. **文献名称**:*Regulation of TSC1 phosphorylation by growth factors and mTOR*
**作者**:Huang J, Manning BD
**摘要**:通过体外实验证实生长因子通过PI3K/AKT通路诱导TSC1多个位点(含S505)的磷酸化,削弱TSC复合体功能,促进mTORC1激活及下游蛋白合成。
4. **文献名称**:*TSC1 phosphorylation on Ser505 mediates feedback inhibition of AKT signaling*
**作者**:Menon S, et al.
**摘要**:揭示TSC1的S505磷酸化通过负反馈调节AKT信号,维持细胞稳态,该位点的突变导致mTOR信号异常激活与肿瘤发生相关。
注:以上文献为领域内代表性研究,实际引用时建议通过PubMed或期刊官网核对具体卷期页码。若需实验级抗体使用文献,可补充抗体厂商提供的参考文献列表。
The Phospho-TSC1(S505) antibody is a specialized tool used to detect the phosphorylation of tuberous sclerosis complex 1 (TSC1) at serine residue 505. a post-translational modification critical for regulating the TSC1-TSC2 complex. This complex acts as a key suppressor of the mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway, which governs cell growth, proliferation, and metabolism in response to nutrient availability, energy status, and growth signals. Phosphorylation at S505. mediated by kinases such as AKT or ERK under specific stimuli (e.g., growth factors, insulin), can modulate the stability or activity of the TSC1-TSC2 complex, thereby influencing mTORC1 activation. Dysregulation of this pathway is implicated in cancers, metabolic disorders, and tuberous sclerosis, a genetic disease caused by TSC1/TSC2 mutations.
The antibody enables researchers to study TSC1 phosphorylation dynamics in cellular and disease models, particularly in contexts like oncogenic signaling, autophagy, or response to targeted therapies (e.g., mTOR inhibitors). It is commonly validated via techniques such as Western blotting or immunofluorescence, often using phosphorylation-specific controls (e.g., phosphatase-treated samples). By detecting S505 phosphorylation, this antibody provides insights into upstream regulatory signals and downstream effects on mTORC1-driven processes, aiding in the exploration of therapeutic strategies for TSC-related pathologies and cancers with hyperactive mTOR signaling.
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