AB5112
抗帕金蛋白，氨基酸305-323
serum, Chemicon®
别名:
Anti-AR-JP, Anti-LPRS2, Anti-PARK2, Anti-PDJ
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关于此项目
UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Conjugate:
unconjugated
Clone:
polyclonal
Application:
ELISA, IHC, WB
Species reactivity:
rat, human
Citations:
21
Technique(s):
ELISA: suitable, immunohistochemistry: suitable, western blot: suitable
Uniprot accession no.:
biological source
rabbit
conjugate
unconjugated
antibody form
serum
antibody product type
primary antibodies
clone
polyclonal
species reactivity
rat, human
manufacturer/tradename
Chemicon®
technique(s)
ELISA: suitable, immunohistochemistry: suitable, western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
dry ice
target post-translational modification
unmodified
Quality Level
Gene Information
human ... PARK2(5071)
Application
使用该抗-Parkin抗体，氨基酸305-323经验证可用于ELISA、WB、IH。
免疫组化： 1:1000 - 1:2000
单位点ELISA
蛋白质印迹：1:1000 - 1:2000（在人类大脑的斑点上识别44-52 kDa的双重序列）
免疫原肽（目录号AG237）可用于预吸收对照。
最佳工作稀释度必须由最终用户进行确定。
单位点ELISA
蛋白质印迹：1:1000 - 1:2000（在人类大脑的斑点上识别44-52 kDa的双重序列）
免疫原肽（目录号AG237）可用于预吸收对照。
最佳工作稀释度必须由最终用户进行确定。
研究子类别
神经退行性疾病
神经退行性疾病
研究类别
神经科学
神经科学
Biochem/physiol Actions
Parkin。帕金森氏病是一种常见的神经退行性疾病，是由于利用神经递质多巴胺的大脑区域（黑质）中的神经元缓慢死亡引起的。Parkin是最近发现的一种编码大蛋白的基因，可能参与细胞中正常和异常蛋白降解。最近的证据表明，Parkin基因的点突变似乎是某些形式的帕金森病的发病机制。
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。
Immunogen
一种19个氨基酸的肽（RILGEEQYNRYQQYGAEEC），对应于人类Parkin蛋白分子的305-323氨基酸。选择内部肽序列以避免与泛素交叉反应的可能性。
表位：氨基酸305-323
Physical form
兔血清。 冻干。用50 μL无菌蒸馏水复溶。离心以除去不溶物。不含防腐剂。
Preparation Note
自收到之日起，冻干材料在-20°C至-70°C下可保存长达12个月。 复溶后，以未稀释的等分试样在-20°C至-70°C下保存长达6个月。 应避免反复冻/融循环。为了获得更高的稳定性，应添加（1：1）甘油（ACS级或更优级）。
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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存储类别
11 - Combustible Solids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
V D'Agata et al.
The European journal of neuroscience, 12(10), 3583-3588 (2000-10-13)
A mutation in the parkin gene has been identified as the cause for an autosomal recessively inherited form of early onset Parkinson's disease. We have recently isolated the mRNA coding for the rat homologue of parkin and showed its widespread
Nilotinib-induced autophagic changes increase endogenous parkin level and ubiquitination, leading to amyloid clearance.
Lonskaya, I; Hebron, ML; Desforges, NM; Schachter, JB; Moussa, CE
Journal of Molecular Medicine null
Irina Lonskaya et al.
EMBO molecular medicine, 5(8), 1247-1262 (2013-06-06)
Tyrosine kinase inhibitors (TKIs) are effective therapies for leukaemia. Alzheimer is a neurodegenerative disease characterized by accumulation of β-amyloid (plaques) and hyper-phosphorylated Tau (tangles). Here we show that AD animals have high levels of insoluble parkin and decreased parkin-Beclin-1 interaction
I Lonskaya et al.
Neuroscience, 232, 90-105 (2012-12-25)
Parkinson's disease (PD) is a motor disorder that involves death of dopaminergic neurons in the substantia nigra pars compacta. Parkin is an autosomal recessive gene that is mutated in early onset PD. We investigated the role of parkin and autophagic
Paola Lenzi et al.
International journal of molecular sciences, 22(10) (2021-06-03)
Glioblastoma (GBM) cells feature mitochondrial alterations, which are documented and quantified in the present study, by using ultrastructural morphometry. Mitochondrial impairment, which roughly occurs in half of the organelles, is shown to be related to mTOR overexpression and autophagy suppression.
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