Your Good Partner in Biology Research

  1. Home
  2. 抗體
  3. 多克隆抗體
  4. PINK1 Antibody

PINK1 Antibody

  • 中文名稱：
    PINK1兔多克隆抗體
  • 貨號：
    CSB-PA447054
  • 規(guī)格：
    ￥1100
  • 其他：

產(chǎn)品詳情

  • Uniprot No.：
  • 基因名：
  • 別名：
    BRPK antibody; FLJ27236 antibody; mitochondrial antibody; PARK 6 antibody; PARK6 antibody; Phosphatase and Tensin Homolog antibody; PINK 1 antibody; PINK1 antibody; PINK1_HUMAN antibody; Protein kinase BRPK antibody; PTEN induced putative kinase 1 antibody; PTEN induced putative kinase protein 1 antibody; PTEN-induced putative kinase protein 1 antibody; Serine/threonine kinase PINK1 mitochondrial antibody; Serine/threonine protein kinase PINK1 mitochondrial antibody; Serine/threonine-protein kinase PINK1 antibody
  • 宿主：
    Rabbit
  • 反應種屬：
    Human,Mouse
  • 免疫原：
    Synthetic peptide of Human PINK1
  • 免疫原種屬：
    Homo sapiens (Human)
  • 標記方式：
    Non-conjugated
  • 抗體亞型：
    IgG
  • 純化方式：
    Antigen affinity purification
  • 濃度：
    It differs from different batches. Please contact us to confirm it.
  • 保存緩沖液：
    -20°C, pH7.4 PBS, 0.05% NaN3, 40% Glycerol
  • 產(chǎn)品提供形式：
  • 應用范圍：
    ELISA
  • 推薦稀釋比：
    Application Recommended Dilution
    ELISA 1:2000-1:5000
  • Protocols：
  • 儲存條件：
    Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
  • 貨期：
    Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.

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：
    1. These results identify a novel role of PINK1 modulating the levels of LRRK2 in Parkinson's disease fibroblasts and neurons. PMID: 27975167
    2. Knockdown of PINK1 suppressed the proliferation, migration, invasion, and induced apoptosis and mitochondrial dysfunction of lung cancer cells. PMID: 29966978
    3. 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
    4. Results describe a novel pathogenic mechanism in recessive Parkinson's disease, where PINK1 deficiency may increase neuron death via exacerbation of inflammatory stimuli-induced nitric oxide production and abnormal innate immune responses in glia cells. PMID: 29321620
    5. The results demonstrate that Nix can serve as an alternative mediator of mitophagy to maintain mitochondrial turnover, identifying Nix as a promising target for neuroprotective treatment in PINK1/Parkin-related Parkinson's disease. PMID: 28281653
    6. Studies indicate a functional PTEN-induced putative kinase 1)(PINK1)/E3 ubiquitin protein ligase (parkin) mitophagy pathway in neurons [Review]. PMID: 29085955
    7. PINK1 detection could help stratify patients who may have poor response to chemotherapy and guide the individual treatment. PMID: 29937472
    8. A mitochondrial protein PINK1 acts as a mitochondrial gatekeeper able to sense the presence of healthy or damaged mitochondria. (Review) PMID: 28647367
    9. mitochondrial dysfunction activates the PINK1/Parkin signaling and mitophagy in renal tubular epithelial cells under albumin overload condition. PMID: 29494565
    10. High Pink1 Expression is Associated with Cancer Progression and Chemo-Resistance in Esophageal Squamous Cell Carcinoma. PMID: 29022200
    11. Hsp70participated in PINK1-mediated mitophagy by stabilizing PINK1. PMID: 29107085
    12. This study showed that the heterozygous Pink1 mutation carriers show subtle motor abnormalities when a detailed, specialized motor examination is applied and compared to mutation-negative matched control subjects. PMID: 28716427
    13. 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
    14. Study confirmed that common variants in PARL and PINK1 were associated with leprosy. Furthermore, PARL and PINK1 could physically interact with each other and were involved in the highly connected network formed by reported leprosy susceptibility genes PMID: 27876828
    15. melatonin stimulates PINK1 expression via an MT2 /Akt/NF-kappaB pathway, and such stimulation is important for the prevention of neuronal cell apoptosis under high glucose conditions. PMID: 28580603
    16. The importance of parkin activation by the PINK1 phosphorylation. PMID: 28007983
    17. Target of PINK1 polyubiquitination is the mature form and is mediated by ubiquitination of a conserved lysine at position 137. PMID: 28683321
    18. that mutant PINK1 p.I368N can not be stabilized on the outer mitochondrial membrane upon mitochondrial stress and due to conformational changes in the active site does not exert kinase activity towards ubiquitin PMID: 28438176
    19. PINK1 mediates the complex balance between polyphyllin I-induced mitophagy and mitochondrial fission-mediated apoptosis in breast cancer cells. PMID: 28060722
    20. Here we review the evidence supporting PINK1/Parkin mitophagy in vivo and its causative role in neurodegeneration, and outline outstanding questions for future investigations. PMID: 28213158
    21. PINK1 utilises a lowly populated yet more suitable C-terminally retracted (Ub-CR) conformation of Ub for efficient phosphorylation. PMID: 29133469
    22. PINK1 was downregulated in the brains of patients with Alzheimer's disease. PMID: 29077793
    23. PINK1 mutation is associated with Alzheimer disease. PMID: 29091718
    24. PINK1 silencing impaired BECN1 enrichment at mitochondria-associated membranes independently of PARK2, suggesting a novel role for PINK1 in regulating mitophagy. PMID: 28368777
    25. an impaired PINK1-PARK2-mediated neuroimmunology pathway contributes to septic death. PMID: 27754761
    26. We demonstrated that miR-27a and miR-27b regulate PINK1 expression and autophagic clearance of damaged mitochondria PMID: 27456084
    27. The effects of variants in the Parkin, PINK1, and DJ-1 genes along with evidence for their pathogenicity have been summarized. (Review) PMID: 26965687
    28. data suggest that ROS may act as a trigger for the induction of Parkin/PINK1-dependent mitophagy. PMID: 28848050
    29. PKA-mediated phosphorylation of MIC60 negatively regulates mitochondrial clearance that is initiated by PINK1 and Parkin. PMID: 27153535
    30. We report that loss of PINK1 contributes to the Warburg effect through ROS-dependent stabilization of hypoxia-inducible factor-1A and reduced pyruvate kinase muscle isozyme 2 activity which highlight the importance of PINK1 and reactive oxygen species balance in normal and tumor cells. PMID: 27325644
    31. PINK1 disease mutants failed to recruit synphilin-1 and did not activate mitophagy, indicating that PINK1-synphilin-1-SIAH-1 represents a new parkin-independent mitophagy pathway. Drugs that activate this pathway will provide a novel strategy to promote the clearance of damaged mitochondria in Parkinson's disease. PMID: 27334109
    32. PINK1 p.G411S is a rare genetic risk factor with a relatively large effect size conferred by a partial dominant-negative function phenotype. PMID: 27807026
    33. In summary, our results demonstrate that PINK1 promoted hepatic IR via JNK and ERK pathway in PA treated HepG2 cells, implying a novel molecular target for the therapy of diabetes. PMID: 27423393
    34. 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
    35. PINK1 interferes with selective mitochondrial fission and mitophagy. PMID: 27091447
    36. findings suggest that PINK1 and PARKIN play critical roles in selective cell death in which damaged mitochondria are retained, independent of mitochondrial autophagy. PMID: 27302064
    37. findings underscore the importance of a mitophagy regulatory network of ATM and PINK1/Parkin and elucidate a novel mechanism by which ATM influences spermidine-induced mitophagy PMID: 27089984
    38. our findings indicate that PINK1 plays a significant role in NSCLC progression and chemoresistance, and highlights its potential role as a target in future anticancer therapies. PMID: 28259921
    39. Association of early onset Parkinson' and severe clinical signs with multiple alterations in PINK1 in Turkish patients. PMID: 27455133
    40. Data suggest that PPARG (peroxisome proliferator-activated receptor gamma) protects against insecticide-induced cytotoxicity/apoptosis by regulating PINK1 (PTEN induced putative kinase 1) expression in neurons, including dopaminergic neurons; the insecticide used in these experiments was deltamethrin; the neuroprotective agent was the hypoglycemic agent, rosiglitazone. PMID: 27553674
    41. These findings pinpoint PINK1-short form as a sensor of proteasomal activities that transduces the proteasomal impairment signal to the aggresome formation machinery. PMID: 27050454
    42. Differential submitochondrial localization of PINK1 serves as a molecular switch for mediating two distinct mitochondrial signaling pathways in maintenance of mitochondrial homeostasis. PMID: 26436374
    43. Processing and shuttling of PINK1 through mitochondria is conformed to at least three possible functional microcompartments for PINK1 activity (I, cytosol; II, outer mitochondrial membrane; III, inside mitochondria). PMID: 26046594
    44. results indicate that PINK1 expression is positively regulated by NRF2 and that the NRF2-PINK1 signaling axis is deeply involved in cell survival. PMID: 26555609
    45. High expression of PARK6 might lead to the occurrence of non-small-cell lung cancer. PMID: 26245297
    46. These results suggest that pyruvate is required for CCCP-induced PINK1/PARK2-mediated mitophagy. PMID: 26071202
    47. PINK1-PARK2 pathway-mediated mitophagy plays a key regulatory role in CSE-induced mitochondrial ROS production and cellular senescence in human bronchial epithelial cells PMID: 25714760
    48. mutant G309D PINK1 significantly reduced phosphorylation of GSK3beta at serine 9, suggesting that alterations in GSK3beta activity play an essential role in mutant G309D PINK1-induced tau phosphorylation at the PHF-1 site PMID: 25899925
    49. TGF-beta1 induces lung epithelial cell mitochondrial ROS and depolarization and stabilizes the key mitophagy initiating protein, PINK1 PMID: 25785991
    50. The results of the combined in silico simulations-based and experimental assay-based study indicates that PINK1-dependent Ser65 phosphorylation of Parkin is required for its activation and triggering of 'opening' conformations. PMID: 25849928

    顯示更多

    收起更多

  • 相關疾?。?/div>
    Parkinson disease 6 (PARK6)
  • 亞細胞定位：
    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：
    Highly expressed in heart, skeletal muscle and testis, and at lower levels in brain, placenta, liver, kidney, pancreas, prostate, ovary and small intestine. Present in the embryonic testis from an early stage of development.
  • 數(shù)據(jù)庫鏈接：

    HGNC: 14581

    OMIM: 168600

    KEGG: hsa:65018

    STRING: 9606.ENSP00000364204

    UniGene: Hs.389171