| 货号 | 2535L |
| 反应种属 | Human/Mouse/Rat/Hamster/Monkey/D.melanogaster/S.cerevisiae |
| 来源宿主 | Rabbit |
| 应用 | W/IP/IHC-P |
| 目标/特异性 | Phospho-AMPKα (Thr172) (40H9) Rabbit mAb detects endogenous AMPKα only when phosphorylated at threonine 172. The antibody detects both α1 and α2 isoforms of the catalytic subunit, but does not detect the regulatory β or γ subunits. |
| 使用方法 | WB(1:1000) IP (1:50) IHC-P (1:100) |
| 供应商 | CST |
| 背景 | AMP-activated protein kinase (AMPK) is highly conserved from yeast to plants and animals and plays a key role in the regulation of energy homeostasis (1). AMPK is a heterotrimeric complex composed of a catalytic α subunit and regulatory β and γ subunits, each of which is encoded by two or three distinct genes (α1, 2; β1, 2; γ1, 2, 3) (2). The kinase is activated by an elevated AMP/ATP ratio due to cellular and environmental stress, such as heat shock, hypoxia, and ischemia (1). The tumor suppressor LKB1, in association with accessory proteins STRAD and MO25, phosphorylates AMPKα at Thr172 in the activation loop, and this phosphorylation is required for AMPK activation (3-5). AMPKα is also phosphorylated at Thr258 and Ser485 (for α1; Ser491 for α2). The upstream kinase and the biological significance of these phosphorylation events have yet to be elucidated (6). The β1 subunit is post-translationally modified by myristoylation and multi-site phosphorylation including Ser24/25, Ser96, Ser101, Ser108, and Ser182 (6,7). Phosphorylation at Ser108 of the β1 subunit seems to be required for the activation of AMPK enzyme, while phosphorylation at Ser24/25 and Ser182 affects AMPK localization (7). Several mutations in AMPKγ subunits have been identified, most of which are located in the putative AMP/ATP binding sites (CBS or Bateman domains). Mutations at these sites lead to reduction of AMPK activity and cause glycogen accumulation in heart or skeletal muscle (1,2). Accumulating evidence indicates that AMPK not only regulates the metabolism of fatty acids and glycogen, but also modulates protein synthesis and cell growth through EF2 and TSC2/mTOR pathways, as well as blood flow via eNOS/nNOS (1). |
| 存放说明 | -20C |
| 计算分子量 | 62 |
Western blot analysis of extracts from C2C12 cells, untreated or oligomycin-treated (0.5 µM), using Phospho-AMPKα (Thr172) (40H9) Rabbit mAb (upper) or AMPKα Antibody #2532 (lower). 对C2C12细胞（未处理，或0.5 ?M 寡霉素处理），使用Phospho-AMPKα (Thr172) (40H9) Rabbit mAb兔单抗（上图）或AMPKα Antibody #2532（下图）进行Western blot分析。 | |
Immunohistochemical analysis of paraffin-embedded NCI-H228 cell pellets, control (left) or phenformin-treated (right), using Phospho-AMPKalpha (T172) (40H9) Rabbit mAb. 对石蜡包埋的NCI-H228颗粒中，对照（左）或phenformin处理（右），使用Phospho-AMPKalpha (T172) (40H9) Rabbit mAb兔单抗进行免疫组化分析。 |
