Anti-Parkin 抗体 (ab15494)
Key features and details
- Rabbit polyclonal to Parkin
- Suitable for: ICC/IF, IHC-P
- Reacts with: Human
- Isotype: IgG
製品の概要
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製品名
Anti-Parkin antibody
Parkin 一次抗体 製品一覧 -
製品の詳細
Rabbit polyclonal to Parkin -
由来種
Rabbit -
アプリケーション
適用あり: ICC/IF, IHC-Pmore details -
種交差性
交差種: Human
交差が予測される動物種: Mouse, Rat -
免疫原
Synthetic peptide within Human Parkin aa 50-150 (N terminal). The exact sequence is proprietary.
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ポジティブ・コントロール
- Recombinant Human Parkin protein (ab114219) can be used as a positive control in WB. IHC-P: Human brain tissue.
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特記事項
This product is FOR RESEARCH USE ONLY. For commercial use, please contact partnerships@abcam.com.
The Life Science industry has been in the grips of a reproducibility crisis for a number of years. Abcam is leading the way in addressing this with our range of recombinant monoclonal antibodies and knockout edited cell lines for gold-standard validation. Please check that this product meets your needs before purchasing.
If you have any questions, special requirements or concerns, please send us an inquiry and/or contact our Support team ahead of purchase. Recommended alternatives for this product can be found below, along with publications, customer reviews and Q&As
製品の特性
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製品の状態
Liquid -
保存方法
Shipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles. -
バッファー
pH: 7.60
Preservative: 0.1% Sodium azide
Constituents: PBS, 1% BSA -
Concentration information loading...
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精製度
Immunogen affinity purified -
ポリ/モノ
ポリクローナル -
アイソタイプ
IgG -
研究分野
関連製品
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Compatible Secondaries
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Isotype control
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Recombinant Protein
アプリケーション
The Abpromise guarantee
Abpromise保証は、 次のテスト済みアプリケーションにおけるab15494の使用に適用されます
アプリケーションノートには、推奨の開始希釈率がありますが、適切な希釈率につきましてはご検討ください。
アプリケーション | Abreviews | 特記事項 |
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ICC/IF |
Use at an assay dependent concentration.
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IHC-P |
1/30. Perform heat mediated antigen retrieval before commencing with IHC staining protocol.
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特記事項 |
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ICC/IF
Use at an assay dependent concentration. |
IHC-P
1/30. Perform heat mediated antigen retrieval before commencing with IHC staining protocol. |
ターゲット情報
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機能
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. -
組織特異性
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). -
パスウェイ
Protein modification; protein ubiquitination. -
関連疾患
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. -
配列類似性
Belongs to the RBR family. Parkin subfamily.
Contains 1 IBR-type zinc finger.
Contains 2 RING-type zinc fingers.
Contains 1 ubiquitin-like domain. -
ドメイン
The ubiquitin-like domain binds the PSMD4 subunit of 26S proteasomes. -
翻訳後修飾
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. -
細胞内局在
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. - Information by UniProt
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参照データベース
- Entrez Gene: 5071 Human
- Entrez Gene: 50873 Mouse
- Entrez Gene: 56816 Rat
- Omim: 602544 Human
- SwissProt: O60260 Human
- SwissProt: Q9WVS6 Mouse
- SwissProt: Q9JK66 Rat
- Unigene: 132954 Human
see all -
別名
- AR JP antibody
- E3 ubiquitin ligase antibody
- E3 ubiquitin protein ligase parkin antibody
see all
画像
データシートおよび資料
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SDS download
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Datasheet download
参考文献 (7)
ab15494 は 7 報の論文で使用されています。
- Lin L et al. Sema3A alleviates viral myocarditis by modulating SIRT1 to regulate cardiomyocyte mitophagy. Environ Toxicol 38:1305-1317 (2023). PubMed: 36880403
- Lai Q et al. Inhibition of KMO Ameliorates Myocardial Ischemia Injury via Maintaining Mitochondrial Fusion and Fission Balance. Int J Biol Sci 19:3077-3098 (2023). PubMed: 37416768
- Koo BH et al. Arginase II protein regulates Parkin-dependent p32 degradation that contributes to Ca2+-dependent eNOS activation in endothelial cells. Cardiovasc Res 118:1344-1358 (2022). PubMed: 33964139
- Ke PY et al. Baicalein Activates Parkin-Dependent Mitophagy through NDP52 and OPTN. Cells 11:N/A (2022). PubMed: 35406696
- Ferrer-Curriu G et al. The protective effect of fibroblast growth factor-21 in alcoholic cardiomyopathy: a role in protecting cardiac mitochondrial function. J Pathol 253:198-208 (2021). PubMed: 33125701
- Zhang X et al. Parkin facilitates proteasome inhibitor-induced apoptosis via suppression of NF-?B activity in hepatocellular carcinoma. Cell Death Dis 10:719 (2019). PubMed: 31558697
- Zhang R et al. Corilagin Alleviates Nonalcoholic Fatty Liver Disease in High-Fat Diet-Induced C57BL/6 Mice by Ameliorating Oxidative Stress and Restoring Autophagic Flux. Front Pharmacol 10:1693 (2019). PubMed: 32116684