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HRPBiotinGoldRBITCAPFITCCy3Cy5Cy5.5Cy7PEPE-Cy3PE-Cy5PE-Cy5.5PE-Cy7APCAlexa Fluor 350Alexa Fluor 488Alexa Fluor 555Alexa Fluor 594Alexa Fluor 647

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HRPBiotinGoldRBITCAPFITCCy3Cy5Cy5.5Cy7PEPE-Cy3PE-Cy5PE-Cy5.5PE-Cy7APCAlexa Fluor 350Alexa Fluor 488Alexa Fluor 555Alexa Fluor 594Alexa Fluor 647

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Anti-phospho-Parkin (Ser65)/PE-Cy3

货号: bs-19882R-PE-Cy3 基本售价: 2980.0 元 规格: 100ul

产品信息

产品编号
bs-19882R-PE-Cy3
英文名称
Anti-phospho-Parkin (Ser65)/PE-Cy3
中文名称
PE-Cy3标记的磷酸化帕金森病蛋白2抗体
别    名
Parkin (phospho S65); p-Parkin (phospho S65); AR JP; E3 ubiquitin ligase; E3 ubiquitin protein ligase parkin; E3 ubiquitin-protein ligase parkin; FRA6E; LPRS 2; LPRS2; PARK 2; PARK2; Parkin 2; Parkinson disease (autosomal recessive juvenile) 2; Parkinson disease (autosomal recessive, juvenile) 2, parkin; Parkinson disease protein 2; Parkinson juvenile disease protein 2; Parkinson protein 2 E3 ubiquitin protein ligase; Parkinson protein 2, E3 ubiquitin protein ligase (parkin); PDJ; PRKN 2; PRKN; PRKN2; PRKN2_HUMAN; Ubiquitin E3 ligase PRKN.  
规格价格
100ul/2980元购买        大包装/询价
说 明 书
100ul  
产品类型
磷酸化抗体 
研究领域
细胞生物  神经生物学  泛素  
抗体来源
Rabbit
克隆类型
Polyclonal
交叉反应
Human, Pig, Cow, Horse, Sheep, Monkey, 
产品应用
ICC=1:50-200 IF=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量
52kDa
性    状
Lyophilized or Liquid
浓    度
1mg/ml
免 疫 原
KLH conjugated synthesised phosphopeptide derived from human Parkin around the phosphorylation site of Ser65.
亚    型
IgG
纯化方法
affinity purified by Protein A
储 存 液
0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存条件
Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
产品介绍
background:
The precise function of this gene is unknown; however, the encoded protein is a component of a multiprotein E3 ubiquitin ligase complex that mediates the targeting of substrate proteins for proteasomal degradation. Mutations in this gene are known to cause Parkinson disease and autosomal recessive juvenile Parkinson disease. Alternative splicing of this gene produces multiple transcript variants encoding distinct isoforms. Additional splice variants of this gene have been described but currently lack transcript support. [provided by RefSeq, Jul 2008]

Function:
Functions within a multiprotein E3 ubiquitin ligase complex, catalyzing the covalent attachment of ubiquitin moieties onto substrate proteins, such as BCL2, SYT11, CCNE1, GPR37, STUB1, a 22 kDa O-linked glycosylated isoform of SNCAIP, SEPT5, ZNF746 and AIMP2. Mediates monoubiquitination as well as Lys-48-linked and Lys-63-linked polyubiquitination of substrates depending on the context. Participates in the removal and/or detoxification of abnormally folded or damaged protein by mediating Lys-63-linked polyubiquitination of misfolded proteins such as PARK7: Lys-63-linked polyubiquitinated misfolded proteins are then recognized by HDAC6, leading to their recruitment to aggresomes, followed by degradation. Mediates Lys-63-linked polyubiquitination of SNCAIP, possibly playing a role in Lewy-body formation. Mediates monoubiquitination of BCL2, thereby acting as a positive regulator of autophagy. Promotes the autophagic degradation of dysfunctional depolarized mitochondria. Mediates Lys-48-linked polyubiquitination of ZNF746, followed by degradation of ZNF746 by the proteasome; possibly playing a role in role in regulation of neuron death. Limits the production of reactive oxygen species (ROS). Loss of this ubiquitin ligase activity appears to be the mechanism underlying pathogenesis of PARK2. May protect neurons against alpha synuclein toxicity, proteasomal dysfunction, GPR37 accumulation, and kainate-induced excitotoxicity. May play a role in controlling neurotransmitter trafficking at the presynaptic terminal and in calcium-dependent exocytosis. Regulates cyclin-E during neuronal apoptosis. May represent a tumor suppressor gene.

Subcellular Location:
Cytoplasm > cytosol. Nucleus. Endoplasmic reticulum. Mitochondrion. Mainly localizes in the cytosol. Co-localizes with SYT11 in neutrites. Co-localizes with SNCAIP in brainstem Lewy bodies. Relocates to dysfunctional mitochondria that have lost the mitochondial membrane potential; recruitement to mitochondria is PINK1-dependent.

Tissue Specificity:
Highly expressed in the brain including the substantia nigra. Expressed in heart, testis and skeletal muscle. Expression is down-regulated or absent in tumor biopsies, and absent in the brain of PARK2 patients. Overexpression protects dopamine neurons from kainate-mediated apoptosis. Found in serum (at protein level).

Post-translational modifications:
Auto-ubiquitinates in an E2-dependent manner leading to its own degradation. Also polyubiquitinated by RNF41 for proteasomal degradation.
S-nitrosylated. The inhibition of PARK2 ubiquitin E3 ligase activity by S-nitrosylation could contribute to the degenerative process in PD by impairing the ubiquitination of PARK2 substrates.

DISEASE:
Defects in PARK2 are a cause of Parkinson disease (PARK) [MIM:168600]. A complex neurodegenerative disorder characterized by bradykinesia, resting tremor, muscular rigidity and postural instability. Additional features are characteristic postural abnormalities, dysautonomia, dystonic cramps, and dementia. The pathology of Parkinson disease involves the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies (intraneuronal accumulations of aggregated proteins), in surviving neurons in various areas of the brain. The disease is progressive and usually manifests after the age of 50 years, although early-onset cases (before 50 years) are known. The majority of the cases are sporadic suggesting a multifactorial etiology based on environmental and genetic factors. However, some patients present with a positive family history for the disease. Familial forms of the disease usually begin at earlier ages and are associated with atypical clinical features.Defects in PARK2 are the cause of Parkinson disease type 2 (PARK2) [MIM:600116]; also known as early-onset parkinsonism with diurnal fluctuation (EPDF) or autosomal recessive juvenile Parkinson disease (PDJ). A neurodegenerative disorder characterized by bradykinesia, rigidity, postural instability, tremor, and onset usually befor 40. It differs from classic Parkinson disease by early DOPA-induced dyskinesia, diurnal fluctuation of the symptoms, sleep benefit, dystonia and hyper-reflexia. Dementia is absent. Pathologically, patients show loss of dopaminergic neurons in the substantia nigra, similar to that seen in Parkinson disease; however, Lewy bodies (intraneuronal accumulations of aggregated proteins) are absent.
Note=Defects in PARK2 may be involved in the development and/or progression of ovarian cancer.

Similarity:
Belongs to the RBR family. Parkin subfamily.
Contains 1 IBR-type zinc finger.
Contains 2 RING-type zinc fingers.
Contains 1 ubiquitin-like domain.

Database links:

Entrez Gene: 530858Cow

Entrez Gene: 5071Human

Entrez Gene: 50873Mouse

Entrez Gene: 56816Rat

Omim: 602544Human

SwissProt: O60260Human

SwissProt: Q9WVS6Mouse

SwissProt: Q9JK66Rat

Unigene: 132954Human

Unigene: 311110Mouse

Unigene: 207194Rat



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.