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ATPase, (Na(+) K(+)) alpha-1 subunit antibody - Fambrough, D. M.; Johns Hopkins School of Medicine

RRID:AB_528092

Antibody ID

AB_528092

Target Antigen

ATPase, (Na(+) K(+)) alpha-1 subunit avian, canine, fish, human, mouse, porcine, rat, torpedo, zebrafish

Proper Citation

(DSHB Cat# a6F, RRID:AB_528092)

Clonality

monoclonal antibody

Comments

consolidated with AB_2314847 on 02/2018 by curator.; Application(s): ELISA,Immunofluorescence,Immunohistochemistry,Immunoprecipitation,Western Blot; Date Deposited: 02/02/1996

Host Organism

mouse

Vendor

DSHB Go To Vendor

Cat Num

a6F

Publications that use this research resource

LRRK2 knockdown in zebrafish causes developmental defects, neuronal loss, and synuclein aggregation.

  • Prabhudesai S
  • J. Neurosci. Res.
  • 2017 Nov 29

Literature context:


Abstract:

Although mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most common cause of genetic Parkinson's disease, their function is largely unknown. LRRK2 is pleiotropic in nature, shown to be involved in neurodegeneration and in more peripheral processes, including kidney functions, in rats and mice. Recent studies in zebrafish have shown conflicting evidence that removal of the LRRK2 WD40 domain may or may not affect dopaminergic neurons and/or locomotion. This study shows that ∼50% LRRK2 knockdown in zebrafish causes not only neuronal loss but also developmental perturbations such as axis curvature defects, ocular abnormalities, and edema in the eyes, lens, and otic vesicles. We further show that LRRK2 knockdown results in significant neuronal loss, including a reduction of dopaminergic neurons. Immunofluorescence demonstrates that endogenous LRRK2 is expressed in the lens, brain, heart, spinal cord, and kidney (pronephros), which mirror the LRRK2 morphant phenotypes observed. LRRK2 knockdown results further in the concomitant upregulation of β-synuclein, PARK13, and SOD1 and causes β-synuclein aggregation in the diencephalon, midbrain, hindbrain, and postoptic commissure. LRRK2 knockdown causes mislocalization of the Na(+) /K(+) ATPase protein in the pronephric ducts, suggesting that the edema might be linked to renal malfunction and that LRRK2 might be associated with pronephric duct epithelial cell differentiation. Combined, our study shows that LRRK2 has multifaceted roles in zebrafish and that zebrafish represent a complementary model to further our understanding of this central protein. © 2016 Wiley Periodicals, Inc.