Recombinant Mouse E3 ubiquitin-protein ligase parkin (Prkn)

中文名稱：

小鼠Prkn重組蛋白
貨號：

CSB-YP893911MO
說明書：

MSDS Datasheet
規(guī)格：
來源：

Yeast
其他：

中文名稱：

小鼠Prkn重組蛋白
貨號：

CSB-EP893911MO-B
說明書：

MSDS Datasheet
規(guī)格：
來源：

E.coli
共軛：

Avi-tag Biotinylated
E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.
其他：

中文名稱：

小鼠Prkn重組蛋白
貨號：

CSB-BP893911MO
說明書：

MSDS Datasheet
規(guī)格：
來源：

Baculovirus
其他：

中文名稱：

小鼠Prkn重組蛋白
貨號：

CSB-MP893911MO
說明書：

MSDS Datasheet
規(guī)格：
來源：

Mammalian cell
其他：

產品詳情
產品評價
相關產品
靶點詳情

產品詳情

純度：

>85% (SDS-PAGE)
基因名：

Prkn
Uniprot No.：

Q9WVS6
別名：

Prkn; Park2; E3 ubiquitin-protein ligase parkin; EC 2.3.2.31; Parkin RBR E3 ubiquitin-protein ligase
種屬：

Mus musculus (Mouse)
蛋白長度：

full length protein
表達區(qū)域：

1-464
氨基酸序列

MIVFVRFNSS YGFPVEVDSD TSILQLKEVV AKRQGVPADQ LRVIFAGKEL PNHLTVQNCD LEQQSIVHIV QRPRRRSHET NASGGDEPQS TSEGSIWESR SLTRVDLSSH TLPVDSVGLA VILDTDSKRD SEAARGPVKP TYNSFFIYCK GPCHKVQPGK LRVQCGTCKQ ATLTLAQGPS CWDDVLIPNR MSGECQSPDC PGTRAEFFFK CGAHPTSDKD TSVALNLITS NRRSIPCIAC TDVRSPVLVF QCNHRHVICL DCFHLYCVTR LNDRQFVHDA QLGYSLPCVA GCPNSLIKEL HHFRILGEEQ YTRYQQYGAE ECVLQMGGVL CPRPGCGAGL LPEQGQRKVT CEGGNGLGCG FVFCRDCKEA YHEGDCDSLL EPSGATSQAY RVDKRAAEQA RWEEASKETI KKTTKPCPRC NVPIEKNGGC MHMKCPQPQC KLEWCWNCGC EWNRACMGDH WFDV
蛋白標簽：

Tag?type?will?be?determined?during?the?manufacturing?process.

The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
產品提供形式：

Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
復溶：

We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
儲存條件：

Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
保質期：

The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
貨期：

Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
注意事項：

Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet ：

Please contact us to get it.

產品評價

靶點詳情

功能：

Functions within a multiprotein E3 ubiquitin ligase complex, catalyzing the covalent attachment of ubiquitin moieties onto substrate proteins. Substrates include SYT11 and VDAC1. Other substrates are BCL2, CCNE1, GPR37, RHOT1/MIRO1, MFN1, MFN2, STUB1, SNCAIP, SEPTIN5, TOMM20, USP30, ZNF746, MIRO1 and AIMP2. Mediates monoubiquitination as well as 'Lys-6', 'Lys-11', '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 a 22 kDa O-linked glycosylated isoform of SNCAIP, possibly playing a role in Lewy-body formation. Mediates monoubiquitination of BCL2, thereby acting as a positive regulator of autophagy. Protects against mitochondrial dysfunction during cellular stress, by acting downstream of PINK1 to coordinate mitochondrial quality control mechanisms that remove and replace dysfunctional mitochondrial components. Depending on the severity of mitochondrial damage and/or dysfunction, activity ranges from preventing apoptosis and stimulating mitochondrial biogenesis to regulating mitochondrial dynamics and eliminating severely damaged mitochondria via mitophagy. Activation and recruitment onto the outer membrane of damaged/dysfunctional mitochondria (OMM) requires PINK1-mediated phosphorylation of both PRKN and ubiquitin. After mitochondrial damage, functions with PINK1 to mediate the decision between mitophagy or preventing apoptosis by inducing either the poly- or monoubiquitination of VDAC1, respectively; polyubiquitination of VDAC1 promotes mitophagy, while monoubiquitination of VDAC1 decreases mitochondrial calcium influx which ultimately inhibits apoptosis. When cellular stress results in irreversible mitochondrial damage, promotes the autophagic degradation of dysfunctional depolarized mitochondria (mitophagy) by promoting the ubiquitination of mitochondrial proteins such as TOMM20, RHOT1/MIRO1, MFN1 and USP30. Preferentially assembles 'Lys-6'-, 'Lys-11'- and 'Lys-63'-linked polyubiquitin chains, leading to mitophagy. The PINK1-PRKN pathway also promotes fission of damaged mitochondria by PINK1-mediated phosphorylation which promotes the PRKN-dependent degradation of mitochondrial proteins involved in fission such as MFN2. This prevents the refusion of unhealthy mitochondria with the mitochondrial network or initiates mitochondrial fragmentation facilitating their later engulfment by autophagosomes. Regulates motility of damaged mitochondria via the ubiquitination and subsequent degradation of MIRO1 and MIRO2; in motor neurons, this likely inhibits mitochondrial intracellular anterograde transport along the axons which probably increases the chance of the mitochondria undergoing mitophagy in the soma. Involved in mitochondrial biogenesis via the 'Lys-48'-linked polyubiquitination of transcriptional repressor ZNF746/PARIS which leads to its subsequent proteasomal degradation and allows activation of the transcription factor PPARGC1A. Limits the production of reactive oxygen species (ROS). Regulates cyclin-E during neuronal apoptosis. In collaboration with CHPF isoform 2, may enhance cell viability and protect cells from oxidative stress. Independently of its ubiquitin ligase activity, protects from apoptosis by the transcriptional repression of p53/TP53. 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. May represent a tumor suppressor gene.
基因功能參考文獻：
1. Parkin functions to blunt excessive CHOP to prevent maladaptive ER stress-induced cell death and adverse cardiac ventricular remodeling. PMID: 28522833
2. data suggested that suppressed Sirt3-Foxo3A-Parkin signaling mediated downregulation of mitophagy may play a vital role in the development of diabetic cardiomyopathy. PMID: 27794418
3. Overexpression of parkin resulted in a significant reduction of total-eNOS and p-eNOS in parallel with the downregulation of ERRalpha (a regulator of eNOS) protein and the enhancement of ERRalpha ubiquitination. PMID: 30244249
4. Parkin mice carrying a deletion in exon 3 display impairments in the main pathway responsible for maintaining BH4 levels in the CNS, an essential cofactor for dopamine synthesis, under inflammatory conditions. Concomitant to this alteration, striatum cells do not upregulate BDNF to confer neuroprotection in LPS-exposed mice, displaying an increased number of mitochondria of smaller size with perinuclear clustering. PMID: 29624777
5. the results indicate that PICK1 is a potent inhibitor of Parkin, and the reduction of PICK1 enhances the protective effect of Parkin. PMID: 29987020
6. PINK1 and PARK2 suppress pancreatic tumorigenesis through control of mitochondrial iron-mediated immunometabolism PMID: 30100261
7. When fed with iron-supplemented diet, DMT1-expressing mice exhibit rather selective accumulation of iron in the substantia nigra but otherwise seem normal. Parkin expression is also enhanced, likely as a neuroprotective response. When DMT1 is overexpressed against a Parkin null background, the double-mutant mice similarly resisted a disease phenotype when fed with iron or manganese, but greater susceptibility to 6-OHDA. PMID: 28695462
8. Bnip3l knockout (bnip3l(-/-)) impaired mitophagy and aggravated cerebral I-R (ischemia-reperfusion) injury in mice, which can be rescued by BNIP3L overexpression. The rescuing effects of BNIP3L overexpression can be observed in park2(-/-) mice, which showed mitophagy deficiency after I-R. PMID: 28820284
9. Parkin acts as a regulator of microtubule system during neuronal aging. PMID: 29040870
10. The expression of PINK1 and Parkin were elevated in white adipose tissue in obese mice. PMID: 29501495
11. crossed Parkin knockouts to the Twinkle-TG mouse in which mtDNA deletions are increased specifically in substantia nigra to determine the effect of increased deletion mutagenesis in the absence of mitochondrial quality control PMID: 28042097
12. These findings reveal parkin-mediated cytoprotective mechanisms against misfolded SOD1 toxicity. PMID: 26563499
13. PARK2-dependent acidic postconditioning -induced mitophagy renders the brain resistant to ischemic injury. PMID: 28103118
14. Our results indicate that strict maternal transmission of mitochondria relies on mitophagy and uncover a collaboration between MUL1 and PARKIN in this process. PMID: 27852436
15. an impaired PINK1-PARK2-mediated neuroimmunology pathway contributes to septic death. PMID: 27754761
16. These findings suggest that insufficient mitophagy-mediated PDGFR/PI3K/AKT activation, which is mainly attributed to reduced PARK2 expression, is a potent underlying mechanism for myofibroblast differentiation and proliferation in fibroblastic foci formation during idiopathic pulmonary fibrosis pathogenesis PMID: 27279371
17. Mfn2 downregulation or the exogenous expression of normal Parkin restored cytosolic Ca(2+) transients in fibroblasts from patients with PARK2 mutations, a catalytically inactive Parkinson's disease (PD)-related Parkin variant had no effect. Parkin is directly involved in regulating ER-mitochondria contacts and provide new insight into the role of the loss of Parkin function in PD development PMID: 27206984
18. Our results provide a molecular explanation for the contribution of Drp1 to the pathogenesis of sporadic Parkinson's disease (PD). These findings indicate that the SNO-Parkin pathway may be a novel therapeutic target to treat PD PMID: 27267045
19. These results suggest a previously unidentified role of parkin in mediating endotoxin-induced endothelial proinflammatory signaling and indicate that it may play a critical role in acute inflammation. PMID: 27693468
20. These studies suggest that changes in intestinal lipid absorption may play a primary role in protection from nutritional stress in Park2 KO mice by preventing HFD-induced weight gain and highlight the need for tissue-specific models to address the role of PARK2 during metabolic stress. PMID: 27166280
21. Parkin negatively regulates the number and connectivity of mitochondria via a Drp1-independent mechanism. PMID: 27181353
22. Parkin-overexpressing cells also showed reductions in apoptotic BAX translocation to the mitochondria and cytochrome c release to the cytosol PMID: 27430567
23. Parkin protects against oxygen-glucose deprivation/reperfusion insult by promoting degradation of Drp1. PMID: 27597885
24. The identification of PINK1 and Parkin as suppressors of an immune-response-eliciting pathway provoked by inflammation suggests new insights into Parkinson's disease pathology. PMID: 27345367
25. p62 are subjected to parkin mediated proteasomal degradation PMID: 26746706
26. A comprehensive analysis of influence of the Parkinson disease-associated genes Parkin and DJ-1 on neurotransmitter receptor expression in mice PMID: 26546471
27. Whereas Parkin has been reported to positively regulate the expression of OPA1 through NEMO, herein we found that PARK2 overexpression did not modify the expression of OPA1. PMID: 26024391
28. In mouse hearts Parkin functions as a stress-induced and developmentally-programmed facilitator of cardiomyocyte mitochondrial turnover. (Review) PMID: 26992930
29. gene deletion results in impaired mitophagy and reduced active transforming growth factor-beta1 PMID: 26921108
30. findings support the notion that BAG2 is an upstream regulator of the PINK1/PARKIN signaling pathway. PMID: 26538564
31. The PINK1-Parkin pathway is activated in response to metabolic stress PMID: 26161534
32. Overexpressed human wild type alpha-synuclein in the substantia nigra was phosphorylated at Ser 129 significantly more in parkin knockout mice, though the total alpha synuclein levels were the same as in wild type mice. PMID: 26099628
33. analysis of two types of mitophagy, a DNM1L-dependent pathway and a PARK2-dependent pathway PMID: 25715097
34. FBXW8 and PARK2 are sequestrated into insolubility by ATXN2 PolyQ expansions, but only FBXW8 expression is dysregulated PMID: 25790475
35. PARK2 function where damaged mitochondria are targeted for degradation via a PARK2/PINK1-mediated mechanism. PMID: 25843045
36. instead of transcriptional reprogramming, fetal cardiomyocyte mitochondria undergo perinatal Parkin-mediated mitophagy and replacement by mature adult mitochondria. Mitophagic mitochondrial removal underlies developmental cardiomyocyte mitochondrial plasticity and metabolic transitioning of perinatal hearts. PMID: 26785495
37. the dysregulation of Parkin-PARIS-PGC-1alpha pathway by metabolic malregulation may contribute to the pathogenesis of Parkinson's disease and metformin might exert a neuroprotective effect on Parkinson's disease via the restoration of parkin PMID: 25779963
38. Data indicates that Parkin regulates mitotic progression and its deficiency results in multiple mitotic defects, genomic instability, and tumorigenesis suggesting a role as tumor suppressor. PMID: 26387737
39. parkin loss impairs mitochondrial biogenesis, leading to declining function of the mitochondrial pool and cell death PMID: 26324925
40. our study demonstrates that BNIP3L, as a substrate of PARK2, promotes mitophagy in the PINK1/PARK2 pathway associated with PD pathogenesis. PMID: 25612572
41. Parkin KO mice had decreased mitophagy, beta-oxidation, mitochondrial respiration, and cytochrome c oxidase activity after acute alcohol treatment. PMID: 26159696
42. These data show that parkin is necessary for the recovery of terminal DA concentrations within tuberoinfundibular neurons following acute MPTP administration. PMID: 25447324
43. Parkin is rare in normal hearts and dispensable for constitutive mitophagic quality control. Ablating Drp1 in adult mouse cardiac myocytes upregulates Parkin, provoking mitophagic mitochondrial depletion that contributes to the lethal cardiomyopathy. PMID: 26038571
44. Results show a tissue-specific mitochondrial defect, present early in life of PARK2-/- mice, mildly affecting respiration, without prominent impact on mitochondrial membrane potential. PMID: 24959870
45. Parkin loss caused mitochondrial dysfunction and affected the pathogenicity but not the levels of mtDNA somatic mutations PMID: 26182419
46. Parkin and the RET signaling cascade converge to control mitochondrial integrity and thereby properly maintain substantia nigra pars compacta dopaminergic neurons and their innervation in the striatum. PMID: 25822020
47. parkin-/- mice may represent a promising animal model to study the early stages of PD and for testing new therapeutic strategies to restore learning and memory and synaptic plasticity impairments in PD. PMID: 25486126
48. Parkin is dispensable for mitochondrial respiration, heart function and neuronal survival in the presence of Drp1-regulated mitophagy. PMID: 25349190
49. Through a direct interaction with Parkin, the HCV core protein suppressed mitophagy by inhibiting Parkin translocation to the mitochondria. PMID: 25244949
50. chronic deletion (KO) and acute knockdown of Parkin have differential responses to APAP-induced mitophagy and liver injury in mice. PMID: 25752611
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亞細胞定位：

Cytoplasm, cytosol. Nucleus. Endoplasmic reticulum. Mitochondrion. Mitochondrion outer membrane. Cell projection, neuron projection. Cell junction, synapse, postsynaptic density. Cell junction, synapse, presynapse.
蛋白家族：

RBR family, Parkin subfamily
組織特異性：

Expressed in all subdivisions of the brain (at protein level). Highly expressed in brainstem, cranial nerve, pontine, cerebellar nuclei, indusium griseum, nuclei reticularis, strata oriens and laccunosum moleculare of the hippocampal CA2 region. Low level
數(shù)據(jù)庫鏈接：

KEGG: mmu:50873

STRING: 10090.ENSMUSP00000063644

UniGene: Mm.311110