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PINK1 encodes a serine/threonine protein kinase that localizes to mitochondria. 再加上，我们可以发PINK1 蛋白 (13) 和 和数多这个蛋白质的别的产品。
Showing 10 out of 237 products:
Human Polyclonal PINK1 Primary Antibody for ELISA, ICC - ABIN249446
Weihofen, Ostaszewski, Minami, Selkoe: Pink1 Parkinson mutations, the Cdc37/Hsp90 chaperones and Parkin all influence the maturation or subcellular distribution of Pink1. in Human molecular genetics 2008
Show all 96 Pubmed References
Human Polyclonal PINK1 Primary Antibody for WB - ABIN151937
Meijer, Karimi-Busheri, Huang, Weinfeld, Young: Pnk1, a DNA kinase/phosphatase required for normal response to DNA damage by gamma-radiation or camptothecin in Schizosaccharomyces pombe. in The Journal of biological chemistry 2002
Show all 5 Pubmed References
Human Polyclonal PINK1 Primary Antibody for WB - ABIN1882117
Rogaeva, Johnson, Lang, Gulick, Gwinn-Hardy, Kawarai, Sato, Morgan, Werner, Nussbaum, Petit, Okun, McInerney, Mandel, Groen, Fernandez, Postuma, Foote: Analysis of the PINK1 gene in a large cohort of cases with Parkinson disease. in Archives of neurology 2004
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Human Polyclonal PINK1 Primary Antibody for SimWes, WB - ABIN152067
Xiong, Wang, Chen, Choo, Ma, Tang, Xia, Jiang, Ronai, Zhuang, Zhang: Parkin, PINK1, and DJ-1 form a ubiquitin E3 ligase complex promoting unfolded protein degradation. in The Journal of clinical investigation 2009
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Human Polyclonal PINK1 Primary Antibody for ELISA, WB - ABIN566297
Liu, Ye, Miller, Yuan, Zhang, Tian, Nie, Imae, Arai, Li, Cheng, Shi: Ablation of ALCAT1 mitigates hypertrophic cardiomyopathy through effects on oxidative stress and mitophagy. in Molecular and cellular biology 2012
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Human Monoclonal PINK1 Primary Antibody for IHC, WB - ABIN2115285
Zhou, Huang, Shao, May, Prou, Perier, Dauer, Schon, Przedborski: The kinase domain of mitochondrial PINK1 faces the cytoplasm. in Proceedings of the National Academy of Sciences of the United States of America 2008
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Human Monoclonal PINK1 Primary Antibody for ICC, IF - ABIN4345677
Ko, Park, Park, Koh: PPAR-γ activation attenuates deltamethrin-induced apoptosis by regulating cytosolic PINK1 and inhibiting mitochondrial dysfunction. in Toxicology letters 2016
Human Polyclonal PINK1 Primary Antibody for WB - ABIN652208
Berthier, Jiménez-Sáinz, Pulido: PINK1 regulates histone H3 trimethylation and gene expression by interaction with the polycomb protein EED/WAIT1. in Proceedings of the National Academy of Sciences of the United States of America 2013
Drosophila CHIP protects against mitochondrial dysfunction by acting downstream of Pink1 in parallel with Parkin (显示 PARK2 抗体)
Maintenance of tissue homeostasis upon reduction of Pink1 or Parkin (显示 PARK2 抗体) appears to result from reduction of age- and stress-induced intestinal stem cell proliferation, in part, through induction of ISC senescence.
activation of endoplasmic reticulum stress by defective mitochondria is neurotoxic in pink1 and parkin (显示 PARK2 抗体) flies and that the reduction of this signalling is neuroprotective, independently of defective mitochondria.
autophosphorylation of PINK1 is essential for the mitochondrial translocation of Parkin (显示 PARK2 抗体) and for subsequent phosphorylation and activation of Parkin (显示 PARK2 抗体).
A pink1 genomic knock-in allele was generated to monitor the dynamic expression pattern of PINK1. The spatiotemporal expression pattern of PINK1 correlates with the cell-type specific mitochondrial clearance or persistence. PINK1 and PARKIN (显示 PARK2 抗体) function epistatically to mediate timely specific mitophagy during Drosophila midgut metamorphosis.
Our data indicate that PINK1 and Parkin (显示 PARK2 抗体) play an important role in FUS (显示 FUS 抗体)-induced neurodegeneration. This study has uncovered a previously unknown link between FUS (显示 FUS 抗体) proteinopathy and PINK1/Parkin (显示 PARK2 抗体) genes, providing new insights into the pathogenesis of FUS (显示 FUS 抗体) proteinopathy.
we show that overexpression of Drosophila Clu (显示 CLU 抗体) complements PINK1, but not parkin (显示 PARK2 抗体), mutant muscles. Thus, Clu (显示 CLU 抗体) is essential for mitochondrial homeostasis and functions in concert with Parkin (显示 PARK2 抗体) and VCP (显示 vcp 抗体) for Marf (显示 MFN2 抗体) degradation to promote damaged mitochondrial clearance.
In addition, a PINK1 mutant, which induced mitochondrial enlargement and had been considered as a Drosophila model of Parkinson's disease (PD), caused fly muscle defects, and the loss of vimar could rescue these defects. Furthermore, we found that the mammalian homolog of Vimar, RAP1GDS1 (显示 RAP1GDS1 抗体), played a similar role in regulating mitochondrial morphology, suggesting a functional conservation of this GEF (显示 SLC2A4RG 抗体) member.
Buffy has a role enhancing the loss of parkin (显示 PARK2 抗体) and suppressing the loss of Pink1 phenotypes in Drosophila
PINK1-dependent mitophagy suppresses neural neurodegeneration by removing damaged mitochondria.
Pink1-depleted zebrafish are the first vertebrate model of PINK1 deficiency with loss of dopaminergic neurons.
Our findings suggest that a lack of pink1 in zebrafish alters many vital and critical pathways in addition to the HIF signaling pathway.
Distinct groups of dopaminergic neurons are sensitive to targeted loss of Pink1 factor in a morphant fish model of toxin-induced Parkinson's disease.
Morpholino-mediated loss of pink1 function in zebrafish profoundly affects the development of dopaminergic neurons in the ventral diencephalon and affects behaviour of the zebrafish larvae, namely their response to tactile stimuli and locomotor behavior.
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
PINK1 mediates the complex balance between polyphyllin I-induced mitophagy and mitochondrial fission-mediated apoptosis in breast cancer cells.
Here we review the evidence supporting PINK1/Parkin (显示 PARK2 抗体) mitophagy in vivo and its causative role in neurodegeneration, and outline outstanding questions for future investigations.
PINK1 utilises a lowly populated yet more suitable C-terminally retracted (Ub-CR) conformation of Ub for efficient phosphorylation.
PINK1 was downregulated in the brains of patients with Alzheimer's disease.
PINK1 mutation is associated with Alzheimer disease.
PINK1 silencing impaired BECN1 (显示 BECN1 抗体) enrichment at mitochondria-associated membranes independently of PARK2 (显示 PARK2 抗体), suggesting a novel role for PINK1 in regulating mitophagy.
an impaired PINK1-PARK2 (显示 PARK2 抗体)-mediated neuroimmunology pathway contributes to septic death.
We demonstrated that miR (显示 MLXIP 抗体)-27a and miR (显示 MLXIP 抗体)-27b regulate PINK1 expression and autophagic clearance of damaged mitochondria
The effects of variants in the Parkin (显示 PARK2 抗体), PINK1, and DJ-1 (显示 PARK7 抗体) genes along with evidence for their pathogenicity have been summarized. (Review)
Loss of Atad3a (显示 ATAD3A 抗体) caused accumulation of Pink1 and activated mitophagy.
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.
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.
study identifies a new role of Dual-AKAP1 (显示 AKAP1 抗体) in regulating mitochondrial trafficking through Miro-2 (显示 RHOT2 抗体), and supports a model in which PINK1 and mitochondrial PKA participate in a similar neuroprotective signaling pathway to maintain dendrite connectivity
Study showed that apoptosis is an important form of cellular degeneration in lipopolysaccharide (LPS (显示 TLR4 抗体)-sensitized hypoxic-ischemic (HI) injury in the immature brain. Loss of PINK1 can protect the immature brain against cell apoptosis induced by LPS (显示 TLR4 抗体)-sensitized HI injury. Moreover, alpha-Syn plays a neuroprotective role in LPS (显示 TLR4 抗体)-sensitized HI brain damage in PINK1-knockout neonatal mice
the results suggest that BNIP3 (显示 BNIP3 抗体) plays a vital role in regulating PINK1 mitochondrial outer membrane localization, the proteolytic process of PINK1 and PINK1/parkin (显示 PARK2 抗体)-mediated mitophagy under physiological conditions.
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
The identification of PINK1 and Parkin (显示 PARK2 抗体) as suppressors of an immune-response-eliciting pathway provoked by inflammation suggests new insights into Parkinson's disease pathology.
PINK1 deficiency causes defects in GFAP (显示 GFAP 抗体)-positive astrogliogenesis during brain development.
This gene encodes a serine/threonine protein kinase that localizes to mitochondria. It is thought to protect cells from stress-induced mitochondrial dysfunction. Mutations in this gene cause one form of autosomal recessive early-onset Parkinson disease.
, PTEN induced putative kinase 1
, PTEN-Induced kinase 1
, PTEN-induced putative kinase 1
, serine/threonine-protein kinase PINK1, mitochondrial
, serine/threonine-protein kinase PINK1, mitochondrial-like
, PTEN-induced putative kinase protein 1
, protein kinase BRPK