Recombinant Mouse Serine/threonine-protein kinase PINK1, mitochondrial (Pink1), partial

中文名稱：

小鼠Pink1重組蛋白
貨號：

CSB-YP859152MO
說明書：

MSDS Datasheet
規(guī)格：
來源：

Yeast
其他：

中文名稱：

小鼠Pink1重組蛋白
貨號：

CSB-EP859152MO
說明書：

MSDS Datasheet
規(guī)格：
來源：

E.coli
其他：

中文名稱：

小鼠Pink1重組蛋白
貨號：

CSB-EP859152MO-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Pink1重組蛋白
貨號：

CSB-BP859152MO
說明書：

MSDS Datasheet
規(guī)格：
來源：

Baculovirus
其他：

中文名稱：

小鼠Pink1重組蛋白
貨號：

CSB-MP859152MO
說明書：

MSDS Datasheet
規(guī)格：
來源：

Mammalian cell
其他：

產(chǎn)品詳情
產(chǎn)品評價
靶點詳情

產(chǎn)品詳情

純度：

>85% (SDS-PAGE)
基因名：

Pink1
Uniprot No.：

Q99MQ3
別名：

Pink1; Serine/threonine-protein kinase PINK1; mitochondrial; EC 2.7.11.1; BRPK; PTEN-induced putative kinase protein 1
種屬：

Mus musculus (Mouse)
蛋白長度：

Partial
蛋白標(biāo)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(chǎn)品提供形式：

Lyophilized powder Warning: in_array() expects parameter 2 to be array, null given in /www/web/cusabio_cn/public_html/caches/caches_template/default/content/show_product_protein.php on line 662
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(fù)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(zhì)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(chǎn)品評價

靶點詳情

功能：

Serine/threonine-protein kinase which protects against mitochondrial dysfunction during cellular stress by phosphorylating mitochondrial proteins such as PRKN and DNM1L, 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. Mediates the translocation and activation of PRKN at the outer membrane (OMM) of dysfunctional/depolarized mitochondria. At the OMM of damaged mitochondria, phosphorylates pre-existing polyubiquitin chains at 'Ser-65', the PINK1-phosphorylated polyubiquitin then recruits PRKN from the cytosol to the OMM where PRKN is fully activated by phosphorylation at 'Ser-65' by PINK1. In damaged mitochondria, mediates the decision between mitophagy or preventing apoptosis by promoting PRKN-dependent poly- or monoubiquitination of VDAC1; polyubiquitination of VDAC1 by PRKN promotes mitophagy, while monoubiquitination of VDAC1 by PRKN decreases mitochondrial calcium influx which ultimately inhibits apoptosis. When cellular stress results in irreversible mitochondrial damage, functions with PRKN to promote clearance of damaged mitochondria via selective autophagy (mitophagy). The PINK1-PRKN pathway also promotes fission of damaged mitochondria by phosphorylating and thus promoting 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. Also promotes mitochondrial fission independently of PRKN and ATG7-mediated mitophagy, via the phosphorylation and activation of DNM1L. Regulates motility of damaged mitochondria by promoting 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. Required for ubiquinone reduction by mitochondrial complex I by mediating phosphorylation of complex I subunit NDUFA10.
基因功能參考文獻(xiàn)：
1. these findings suggest that CHIP plays a role in negative regulation of PINK1 stability and may suppress PINK1's cytoprotective effect during staurosporine-induced mammalian cell death. PMID: 29242192
2. The data supports an indispensable role for Mule in cardiac homeostasis through the regulation of mitochondrial function via maintenance of Pgc-1alpha and Pink1 expression and persistent negative regulation of c-Myc. PMID: 28148912
3. these data suggest that alleviation of the sustained mitochondrial dysfunction and oxidative stress through co-modulation of NRF2 and PINK1 may be in charge of restoration of the cognitive impairments in a mouse model of high-LET carbon ion irradiation PMID: 29689442
4. This paper's findings delineate a mechanism by which PINK1 regulates mitochondrial Ca(2+) level through LETM1 and suggest a model by which PINK1 loss leads to deficient phosphorylation of LETM1 and impaired mitochondrial Ca(2+) transport. PMID: 29123128
5. PINK1 and PARK2 suppress pancreatic tumorigenesis through control of mitochondrial iron-mediated immunometabolism PMID: 30100261
6. This study demonstrated that in the Pink1-/- mouse showed disorder of vocalization and sensorimotor function. PMID: 29229503
7. reveal a direct molecular link between nitrosative stress, S-nitrosylated PINK1 formation, and mitophagic dysfunction that contributes to the pathogenesis of Parkinson's disease PMID: 29166608
8. In mitochondria from Pink1(-/-) mice, there was a decrease in free chloride and in free supercomplexes in cultured neurons. PMID: 28408307
9. These findings provide evidence for a novel mechanism underlying the protective effects of PINK1 against alpha-syn-induced neurodegeneration and highlight a novel therapeutic target for Parkinson's disease treatment. PMID: 28933786
10. The results of this study identify PINK1 deficiency as an early modulator of innate immunity in neurons, which precedes late stages of neuroinflammation during alpha-synuclein spreading. PMID: 28768533
11. The expression of PINK1 and Parkin were elevated in white adipose tissue in obese mice. PMID: 29501495
12. LncRNA NEAT1 promoted the MPTP-induced autophagy in PD through stabilization of PINK1 protein. PMID: 29287722
13. Loss of Atad3a caused accumulation of Pink1 and activated mitophagy. PMID: 29242539
14. PTEN-induced putative kinase 1 interacts with and phosphorylates serines 322 and 613 of PARIS to control its ubiquitination and clearance by parkin. PINK1 phosphorylation of PARIS alleviates PARIS toxicity, as well as repression of PGC-1alpha promoter activity. PMID: 28122242
15. Findings highlight a novel mechanism by which PINK1-dependent signalling promotes the rescue of amyloid pathology and amyloid-beta-mediated mitochondrial and synaptic dysfunctions in a transgenic mouse Alzheimer's disease model. PMID: 29077793
16. an impaired PINK1-PARK2-mediated neuroimmunology pathway contributes to septic death. PMID: 27754761
17. These results reveal a new and important relationship between mitochondrial dysfunction and impaired adult hippocampal neurogenesis in a genetic Parkinson's disease model. PMID: 28325755
18. study identifies a new role of Dual-AKAP1 in regulating mitochondrial trafficking through Miro-2, and supports a model in which PINK1 and mitochondrial PKA participate in a similar neuroprotective signaling pathway to maintain dendrite connectivity PMID: 28556983
19. Study showed that apoptosis is an important form of cellular degeneration in lipopolysaccharide (LPS-sensitized hypoxic-ischemic (HI) injury in the immature brain. Loss of PINK1 can protect the immature brain against cell apoptosis induced by LPS-sensitized HI injury. Moreover, alpha-Syn plays a neuroprotective role in LPS-sensitized HI brain damage in PINK1-knockout neonatal mice PMID: 27742469
20. the results suggest that BNIP3 plays a vital role in regulating PINK1 mitochondrial outer membrane localization, the proteolytic process of PINK1 and PINK1/parkin-mediated mitophagy under physiological conditions. PMID: 27528605
21. lack of PINK1 causes increased excitatory transmission and neurotransmitter release in the hippocampus, which might lead to the cognitive decline often observed in Parkinson's disease PMID: 26850695
22. 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
23. PINK1 deficiency causes defects in GFAP-positive astrogliogenesis during brain development. PMID: 26746235
24. The findings of this study show a CB1R dysfunction at corticostriatal synapses in PINK1(-/-), but not in PINK1(+/-) mice, and provide a mechanistic link to the distinct plasticity deficits observed in both genotypes. PMID: 26498506
25. Loss of PINK1 inhibits Ca2+ efflux by NCLX and triggers mitochondrial depolarization. PMID: 26440884
26. PINK1 gene knockout can protect neonatal mice from hypoxic-ischemic brain damage (HIBD). PMID: 26975827
27. Loss of Pink1 reprograms glucose metabolism through HIF1alpha, sustaining increased cell proliferation. PMID: 25058378
28. findings support the notion that BAG2 is an upstream regulator of the PINK1/PARKIN signaling pathway. PMID: 26538564
29. Interplay between E2F1, miR421 and Pink1 regulates mitochondrial morphology and cardiomyocyte death. Pink1 reduces mitochondrial fragmentation and protects cardiomyocyte from apoptosis. PMID: 26184432
30. data suggest that Parkin recruitment to depolarized cardiac mitochondria and subsequent activation of mitophagy is independent of PINK1. PMID: 26110811
31. The PINK1-Parkin pathway is activated in response to metabolic stress PMID: 26161534
32. TGF-beta1 induces lung epithelial cell mitochondrial ROS and depolarization and stabilizes the key mitophagy initiating protein, PINK1 PMID: 25785991
33. our study demonstrates that BNIP3L, as a substrate of PARK2, promotes mitophagy in the PINK1/PARK2 pathway associated with PD pathogenesis. PMID: 25612572
34. Cytosolic PINK1 is stabilized by TRAF6/NF-kappaB activation via Lys-63-linked ubiquitination. PMID: 25987559
35. Loss of PGAM5 disables PINK1-mediated mitophagy in vitro and leads to dopaminergic neurodegeneration and mild dopamine loss in vivo causing a Parkinson's-like movement disorder. PMID: 25222142
36. results demonstrate that total loss of PINK1 leads to an increased sensitivity to alpha-synuclein-induced neuropathology and cell death in vivo PMID: 25037286
37. our study confirmed that SNCA-triggered neurotoxicity is exacerbated by the absence of PINK1 and identified a novel molecular signature that is detectable early in the course of this double pathology. PMID: 25296918
38. PINK1 counteracts the neurotoxicity of PINK1 counteracts the neurotoxicity of mutant Htt. PMID: 25611391
39. This study examines changes in the proteome and phosphoproteome of the PINK1 knockout mouse brain PMID: 25626353
40. PINK1-dependent recruitment of nNOS and its activation in the induction of Parkin translocation takes place in mitophagy. PMID: 25716315
41. mitochondrial respiratory chain defects may be associated with parkinson disease pathogenesis caused by mutations in the PINK1 gene. PMID: 25092611
42. results indicate that DJ1 regulates cell metabolism and proliferation through Pink1 PMID: 25670069
43. Cells lacking Pink1 were more sensitive to cell death induced by C2-Ceramide. In the same cell lines, mitochondrial morphology was fragmented by forskolin. Pink1 may exert a neuroprotective role in part by limiting mitochondrial fission. PMID: 24792327
44. Parkin knockout, Pink1 knockout, DJ-1 knockout and LRRK2 R1441G transgenic mice, were investigated for striatal dopamine levels. PMID: 24733019
45. data indicate that PINK1 deficiency results in swollen, dysfunctional mitochondria and defective mitophagy, and promotes fibrosis in the aging lung. PMID: 25562319
46. The work positions smARF upstream of PINK1 and Parkin and demonstrates that mitophagy can be triggered by intrinsic signaling cascades. PMID: 25217637
47. data indicate that the formation of Lys-63-linked polyubiquitin chains on depolarized mitochondria is not a key factor for the PINK1-Parkin pathway as was once thought. PMID: 25336644
48. PINK1 phosphorylates CLS1 to control CLS1 degradation. PMID: 24703837
49. The PINK1-Parkin-mediated pathway is required for local mitophagy in distal axons in response to focal damage. PMID: 25154397
50. BAG5 protects against mitochondrial oxidative damage through regulating PINK1 degradation. PMID: 24475098
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亞細(xì)胞定位：

Mitochondrion outer membrane; Single-pass membrane protein. Mitochondrion inner membrane; Single-pass membrane protein. Cytoplasm, cytosol.
蛋白家族：

Protein kinase superfamily, Ser/Thr protein kinase family
組織特異性：

High levels expressed in testis, lower levels in brain, heart, lung, liver and kidney.
數(shù)據(jù)庫鏈接：

KEGG: mmu:68943

STRING: 10090.ENSMUSP00000030536

UniGene: Mm.18539