Use your antibodies-online credentials, if available.
PINK1 encodes a serine/threonine protein kinase that localizes to mitochondria. 再加上，我们可以发PINK1 蛋白 (13) 和 PINK1 试剂盒 (3)和数多这个蛋白质的别的产品。
Showing 10 out of 256 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
Show all 4 Pubmed References
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
Show all 3 Pubmed References
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
Show all 2 Pubmed References
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
Show all 2 Pubmed References
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
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
This study found learning and memory abnormalities in PINK1 mutant genotypes in Drosophila.
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-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.
mitochondrial dysfunction activates the PINK1/Parkin (显示 PARK2 抗体) signaling and mitophagy in renal tubular epithelial cells under albumin (显示 ALB 抗体) overload condition.
High Pink1 Expression is Associated with Cancer Progression and Chemo-Resistance in Esophageal Squamous Cell Carcinoma.
Hsp70participated in PINK1-mediated mitophagy by stabilizing PINK1.
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.
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.
Study confirmed that common variants in PARL (显示 PARL 抗体) and PINK1 were associated with leprosy. Furthermore, PARL (显示 PARL 抗体) and PINK1 could physically interact with each other and were involved in the highly connected network formed by reported leprosy susceptibility genes
melatonin stimulates PINK1 expression via an MT2 (显示 MT2 抗体) /Akt (显示 AKT1 抗体)/NF-kappaB (显示 NFKB1 抗体) pathway, and such stimulation is important for the prevention of neuronal cell apoptosis under high glucose conditions.
The importance of parkin (显示 PARK2 抗体) activation by the PINK1 phosphorylation.
Target of PINK1 polyubiquitination is the mature form and is mediated by ubiquitination of a conserved lysine at position 137.
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 and PARK2 (显示 PARK2 抗体) suppress pancreatic tumorigenesis through control of mitochondrial iron-mediated immunometabolism
This study demonstrated that in the Pink1-/- mouse showed disorder of vocalization and sensorimotor function.
reveal a direct molecular link between nitrosative stress, S-nitrosylated PINK1 formation, and mitophagic dysfunction that contributes to the pathogenesis of Parkinson's disease
In mitochondria from Pink1(-/-) mice, there was a decrease in free chloride and in free supercomplexes in cultured neurons.
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.
The expression of PINK1 and Parkin (显示 PARK2 抗体) were elevated in white adipose tissue in obese mice.
LncRNA NEAT1 promoted the MPTP (显示 PTPN2 抗体)-induced autophagy in PD through stabilization of PINK1 protein.
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.
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