产品名称
抗磷酸化ITCH(pT222)抗体, Chemicon®, from rabbit
biological source
rabbit
antibody form
affinity purified immunoglobulin
antibody product type
primary antibodies
clone
polyclonal
purified by
affinity chromatography
species reactivity
human
manufacturer/tradename
Chemicon®
technique(s)
dot blot: suitable
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
phosphorylation (pThr222)
Quality Level
Gene Information
human ... ITCH(83737)
Application
研究子类别
泛素 & 泛素代谢
泛素 & 泛素代谢
研究类别
蛋白运输
蛋白运输
蛋白质印迹：建议稀释度1 - 5 μg/ml
斑点印迹：
斑点印迹：
该抗磷酸化ITCH（pT222）抗体经验证可用于DB、WB 中检测磷酸化ITCH（pT222）。
Biochem/physiol Actions
苏氨酸222（T222）磷酸化的 人ITCH。
Disclaimer
除非我们的产品目录或产品附带的其他公司文档另有说明，否则我们的产品仅供研究使用，不得用于任何其他目的，包括但不限于未经授权的商业用途、体外诊断用途、离体或体内治疗用途或任何类型的消费或应用于人类或动物。
General description
ITCH是一种E3泛素-蛋白连接酶，可以硫酯形式的E2泛素结合酶接受泛素，然后将泛素直接转移至目标底物。ITCH 调节多种转录因子（包括造血转录因子NF-E2）的转录活性，并且可能在免疫反应的调节中起重要作用。ITCH 可使B细胞信号传导中Epstein-Barr病毒LMP2A 活性下调，也与NOTCH1、OCLN、JUN和 JUNB相互作用。ITCH 的组织分布广泛，并位于细胞核与细胞质内 。研究人员描述过两个 ITCH 剪接变体：一个大约103 kDa的形式以及缺少蛋白质N末端一半的42个氨基酸的截短型（~98 kDa）。ITCH 含有一个MAPIM结合位点，其活性受到JNK1引起的多个苏氨酸残基的磷酸化调节。
Immunogen
合成肽，对应于人 ITCH 的一部分，包括222位磷酸化的苏氨酸（PPPpTPRRP）。
Other Notes
浓度：请参考批次特异性浓缩物的检验报告。
Physical form
亲和纯化的免疫球蛋白。溶于含0.1%叠氮化钠的Tris-柠檬酸/磷酸盐缓冲液（pH 7至-8）的液体
Preparation Note
自收到之日起，在2-8°C可最多保存12个月。
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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存储类别
12 - Non Combustible Liquids
wgk
WGK 2
flash_point_f
Not applicable
flash_point_c
Not applicable
William J Sullivan et al.
Cell, 175(1), 117-132 (2018-09-11)
The metabolic state of a cell is influenced by cell-extrinsic factors, including nutrient availability and growth factor signaling. Here, we present extracellular matrix (ECM) remodeling as another fundamental node of cell-extrinsic metabolic regulation. Unbiased analysis of glycolytic drivers identified the
Lin Deng et al.
Journal of virology, 96(6), e0181121-e0181121 (2022-01-20)
We previously reported that hepatitis C virus (HCV) infection activates the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) signaling pathway. However, the roles of ROS/JNK activation in the HCV life cycle remain unclear. We sought to identify a novel role
TMEM55B links autophagy flux, lysosomal repair, and TFE3 activation in response to oxidative stress.
Eutteum Jeong et al.
Nature communications, 15(1), 93-93 (2024-01-04)
Lysosomes have emerged as critical regulators of cellular homeostasis. Here we show that the lysosomal protein TMEM55B contributes to restore cellular homeostasis in response to oxidative stress by three different mechanisms: (1) TMEM55B mediates NEDD4-dependent PLEKHM1 ubiquitination, causing PLEKHM1 proteasomal
Nikolaos Charlaftis et al.
The EMBO journal, 33(21), 2581-2596 (2014-09-28)
Unlike the other MAP3Ks, MEKK1 (encoded by Map3k1) contains a PHD motif. To understand the role of this motif, we have created a knockin mutant of mouse Map3k1 (Map3k1(m) (PHD)) with an inactive PHD motif. Map3k1(m) (PHD) ES cells demonstrate
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