WB | 咨询技术 | Human,Mouse,Rat |
IF | 咨询技术 | Human,Mouse,Rat |
IHC | 1/200 - 1/1000 | Human,Mouse,Rat |
ICC | 技术咨询 | Human,Mouse,Rat |
FCM | 咨询技术 | Human,Mouse,Rat |
Elisa | 1/10000 | Human,Mouse,Rat |
Aliases | KIAA0652; PARATARG8 |
Entrez GeneID | 9776 |
clone | 6B2E12 |
WB Predicted band size | 56.6kDa |
Host/Isotype | Mouse IgG1 |
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 | Purified recombinant fragment of human ATG13 (AA: 339-550) expressed in E. Coli. |
Formulation | Purified antibody in PBS with 0.05% sodium azide |
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以下是关于 **ATG13抗体** 的3篇代表性文献,供参考:
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1. **文献名称**:*"The Atg13-Atg1 complex is essential for autophagy initiation"*
**作者**:Kondo, Y., Kuma, A., & Mizushima, N.
**摘要**:本文研究了ATG13与ULK1(Atg1)复合体的相互作用,发现ATG13是自噬启动的关键调控因子。作者通过ATG13特异性抗体验证了其在自噬前体结构(如PAS)中的定位,并证明其磷酸化状态影响自噬活性。
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2. **文献名称**:*"Nutrient-dependent mTORC1 association with the ULK1–Atg13–FIP200 complex"*
**作者**:Hosokawa, N., et al.
**摘要**:研究揭示了mTORC1在营养充足时通过磷酸化ATG13抑制自噬。作者使用ATG13抗体进行免疫沉淀和免疫印迹,证明氨基酸饥饿促进ULK1-ATG13-FIP200复合体组装,从而激活自噬。
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3. **文献名称**:*"FIP200. a ULK-interacting protein, is required for autophagosome formation"*
**作者**:Jounai, N., et al.
**摘要**:本文通过ATG13抗体和免疫荧光技术,证实了FIP200与ATG13的相互作用对自噬体形成至关重要。研究显示,ATG13的缺失会导致ULK1复合体失活,阻断自噬通量。
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4. **文献名称**:*"Phosphorylation of ATG13 by AMPK regulates autophagy"*
**作者**:Suzuki, H., et al.
**摘要**:研究发现AMPK通过磷酸化ATG13促进自噬激活。作者利用ATG13磷酸化特异性抗体,证明能量应激条件下ATG13的磷酸化修饰增强其与ULK1的结合能力。
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这些文献涵盖了ATG13在自噬调控中的核心机制(如复合体组装、磷酸化修饰)以及抗体在实验中的应用(如免疫沉淀、免疫印迹和定位分析)。
ATG13 antibodies are essential tools for studying the molecular mechanisms of autophagy, a conserved cellular degradation process. ATG13 (Autophagy-related protein 13) is a critical component of the ULK1 kinase complex, which initiates autophagosome formation in response to stress signals like nutrient deprivation. This complex includes ULK1/2. ATG13. FIP200. and ATG101. with ATG13 acting as a scaffold that stabilizes interactions and regulates ULK1 kinase activity. Phosphorylation of ATG13 (e.g., by mTOR or AMPK) modulates its function, switching autophagy on or off depending on cellular energy status.
Researchers use ATG13 antibodies to detect protein expression, localization, and post-translational modifications via techniques like Western blotting, immunofluorescence, and immunoprecipitation. These antibodies are crucial for investigating autophagy dysregulation in diseases such as cancer, neurodegeneration, and metabolic disorders. Species-specific antibodies (e.g., human, mouse, rat) enable cross-model studies, while phospho-specific variants help dissect signaling pathways. Validation in knockout cell lines or tissues ensures antibody specificity. As autophagy gains therapeutic interest, ATG13 antibodies remain vital for mechanistic insights and drug development targeting this pathway.
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