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PINK1 encodes a serine/threonine protein kinase that localizes to mitochondria. Additionally we are shipping PINK1 Proteins (12) and and many more products for this protein.
Showing 10 out of 175 products:
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 references for ABIN1882117
Human Polyclonal PINK1 Primary Antibody for EIA, IHC (p) - ABIN358994
Hatano, Li, Sato, Asakawa, Yamamura, Tomiyama, Yoshino, Asahina, Kobayashi, Hassin-Baer, Lu, Ng, Rosales, Shimizu, Toda, Mizuno, Hattori: Novel PINK1 mutations in early-onset parkinsonism. in Annals of neurology 2004
Show all 2 references for ABIN358994
Rat (Rattus) Polyclonal PINK1 Primary Antibody for ELISA, WB - ABIN334460
Chishti, Bohlega, Ahmed, Loualich, Carroll, Sato, St George-Hyslop, Westaway, Rogaeva: T313M PINK1 mutation in an extended highly consanguineous Saudi family with early-onset Parkinson disease. in Archives of neurology 2006
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
Clu (show CLU Antibodies) directly modulates mitochondrial function, and that Clu's function contributes to the PINK1-Park pathway of mitochondrial quality control.
Human Mask homolog ANKHD1 (show ANKHD1 Antibodies) may serve as a potential therapeutic target for treating Parkinson disease caused by pink1/parkin (show PARK2 Antibodies) mutations.
Various ways of stimulation of the ETC (genetic, pharmacologic and mechanical) (Figure 1) all improve a Pink1 fly model.
These results indicate that the in vivo rescue is due to restoring CI activity rather than promoting mitophagy Our findings support the emerging view that PINK1 plays a role in regulating complex I activity separate from its role with Parkin (show PARK2 Antibodies) in mitophagy
MUL1 (show MUL1 Antibodies) acts in parallel to the PINK1/parkin (show PARK2 Antibodies) pathway on a shared target mitofusin (show MFN2 Antibodies) to maintain mitochondrial integrity.
PINK1-mediated phosphorylation of Miro inhibits synaptic growth and protects dopaminergic neurons in Drosophila.
PINK1 cooperates with Parkin to promote hnRNP-F/Glo ubiquitination and nRCC mRNA translation.
results strongly circumscribe the possible mechanisms of PINK1 action in the mitochondrial life cycle
PINK1 counteracts the neurotoxicity of PINK1 counteracts the neurotoxicity of mutant Htt (show HTT Antibodies).
Parkin (show PARK2 Antibodies) phosphorylation by PINK1 drives Parkin (show PARK2 Antibodies) E3 activity. endogenous PINK1 precisely controls Parkin (show PARK2 Antibodies) activity to maintain the mitochondrial function in muscle tissue and the neuronal function in dopaminergic neurons.
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.
Differential submitochondrial localization of PINK1 serves as a molecular switch for mediating two distinct mitochondrial signaling pathways in maintenance of mitochondrial homeostasis.
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).
pathogenic PINK1 mutants which are not cleaved by PARL (show PARL Antibodies) affect PINK1 kinase activity and the ability to induce PARK2 (show PARK2 Antibodies)-mediated mitophagy.
results indicate that PINK1 expression is positively regulated by NRF2 (show GABPA Antibodies) and that the NRF2 (show GABPA Antibodies)-PINK1 signaling axis is deeply involved in cell survival.
High expression of PARK6 might lead to the occurrence of non-small-cell lung cancer.
These results suggest that pyruvate is required for CCCP-induced PINK1/PARK2 (show PARK2 Antibodies)-mediated mitophagy.
PINK1-PARK2 (show PARK2 Antibodies) pathway-mediated mitophagy plays a key regulatory role in CSE-induced mitochondrial ROS (show ROS1 Antibodies) production and cellular senescence in human bronchial epithelial cells
Rab8A (show RAB8A Antibodies) GTPase (show RACGAP1 Antibodies) Ser (show SIGLEC1 Antibodies)(111) phosphorylation is not directly regulated by PINK1 in vitro and demonstrate in cells the time course of Ser (show SIGLEC1 Antibodies)(111) phosphorylation of Rab8A (show RAB8A Antibodies), 8B and 13 is markedly delayed compared to phosphorylation of Parkin (show PARK2 Antibodies) at Ser (show SIGLEC1 Antibodies)(65).
mutant G309D PINK1 significantly reduced phosphorylation of GSK3beta (show GSK3b Antibodies) at serine 9, suggesting that alterations in GSK3beta (show GSK3b Antibodies) activity play an essential role in mutant G309D PINK1-induced tau phosphorylation at the PHF-1 (show PHF1 Antibodies) site
TGF-beta1 (show TGFB1 Antibodies) induces lung epithelial cell mitochondrial ROS (show ROS1 Antibodies) and depolarization and stabilizes the key mitophagy initiating protein, PINK1
PINK1 deficiency causes defects in GFAP (show GFAP Antibodies)-positive astrogliogenesis during brain development.
The findings of this study show a CB1R (show CNR1 Antibodies) 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.
Loss of PINK1 inhibits Ca2 (show CA2 Antibodies)+ efflux by NCLX (show SLC24A6 Antibodies) and triggers mitochondrial depolarization.
PINK1 gene knockout can protect neonatal mice from hypoxic-ischemic brain damage (HIBD).
Loss of Pink1 reprograms glucose metabolism through HIF1alpha (show HIF1A Antibodies), sustaining increased cell proliferation.
findings support the notion that BAG2 (show BAG2 Antibodies) is an upstream regulator of the PINK1/PARKIN (show PARK2 Antibodies) signaling pathway.
Interplay between E2F1 (show E2F1 Antibodies), miR421 and Pink1 regulates mitochondrial morphology and cardiomyocyte death. Pink1 reduces mitochondrial fragmentation and protects cardiomyocyte from apoptosis.
data suggest that Parkin (show PARK2 Antibodies) recruitment to depolarized cardiac mitochondria and subsequent activation of mitophagy is independent of PINK1.
The PINK1-Parkin (show PARK2 Antibodies) pathway is activated in response to metabolic stress
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