phospho-Parkin (Ser131)抗体特异性结合抗原：抗体本身不能直接溶解或杀伤带有特异抗原的靶细胞，通常需要补体或吞噬细胞等共同发挥效应以**病原微生物或导致病理损伤。然而，抗体可通过与病毒或**的特异性结合，直接发挥中和病毒的作用。
产品编号xy- 19881R
英文名称phospho-Parkin (Ser131)
中文名称磷酸化帕金森病蛋白2抗体
别 名Parkin (phospho S131); p-Parkin (phospho S131); 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.
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
phospho-Parkin (Ser131)抗体交叉反应 Human, Cow,
产品应用WB=1:500-2000 ELISA=1:500-1000 IHC-P=1:400-800 IHC-F=1:400-800 ICC=1:100-500 IF=1:100-500 （石蜡切片需做抗原修复）
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量52kDa
细胞定位细胞核 细胞浆
性 状Lyophilized or Liquid
浓 度1mg/1ml
免 疫 原KLH conjugated synthesised phosphopeptide derived from human Parkin around the phosphorylation site of Ser131.:KD(p-S)PP
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.
phospho-Parkin (Ser131)抗体保存条件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.
PubMedPubMed
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.
Gene ID:
5071
phospho-Parkin (Ser131)抗体（antibody,
Ab）是由效应B细胞（效应**B细胞）分泌，机体用于抵御外来物质，如病毒，**等抗原，结构呈“Y”字型的球状蛋白质，仅仅存在于脊椎动物的血液和B**细胞膜表面。凡是能够跟抗体结合的物质，均被称作抗原，因此对于抗抗体（能够结合抗体的抗体）来说，抗体本身也是一种抗原物质。
phospho-Parkin (Ser131)抗体普通抗体重链和轻链的结构
重链结构：普通的**球蛋白具有2条重链（H链），分子量约为50kD,有μ、δ、γ、ε和α五种重链亚型，对应的**球蛋白名称分别为IgM、IgG、IgA、IgD和IgE。
轻链结构： 普通**球蛋白具有2条轻链（L链），分子质量约25kDa，有κ链和λ链两种亚型，这两种轻链决定了Ig的亚型类别（IgG1，IgG2，IgG3，IgG4）。一个天然的Ig分子两条轻链总是相同的，但在同一个体内可存在分别带有κ或λ链的抗体分子。不同种属生物体内两型轻链的比例不同，正常人血清**球蛋白κ链：λ链约为2：1，而在小鼠的比例为20：1。
2.2抗体Fab段和Fc段
IgG经木瓜蛋白酶酶切后裂解为2个完全相同的Fab段和1个Fc段,每个Fab段都为单价,可与抗原结合但不会再发生凝集反应；经胃蛋白酶酶切后裂解为1个完整F(ab)2片段和碎片化的Fc片段,F(ab’)2片段为双价,可同时结合两个抗原表位。Fab段为抗原结合片段（fragment of antigen binding，Fab），相当于抗体分子的两个臂，由一个完整的轻链和重链的VH和CH1结构域组成。Fc段为可结晶段（fragment crystallizable，Fc）相当于Ig的CH2和CH3结构域，是Ig与效应分子或者细胞相互作用的部位。Fab段包含完整的可变区，以及恒定区的CH1区域。Fc段仅指Ig恒定区CH2和CH3的区域，相当于Y字结构下面那一部分。
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