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AB5112

Sigma-Aldrich

Anti-Parkin Antibody, a.a. 305-323

serum, Chemicon®

Synonyme(s) :

Anti-AR-JP, Anti-LPRS2, Anti-PARK2, Anti-PDJ

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About This Item

Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

Forme d'anticorps

serum

Type de produit anticorps

primary antibodies

Clone

polyclonal

Espèces réactives

rat, human

Fabricant/nom de marque

Chemicon®

Technique(s)

ELISA: suitable
immunohistochemistry: suitable
western blot: suitable

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... PARK2(5071)

Spécificité

Parkin. Parkinson′s disease is a common neurodegenerative disease is caused by slow death of neurons in the substantial nigra, a brain region that utilizes the neurotransmitter dopamine. Parkin, a recently discovered gene encoding a large protein, may be involved in normal and abnormal protein degradation in cells. Recent evidence indicates that point mutations in the Parkin gene appear to be responsible for the pathogenesis of some forms of Parkinson′s disease.

Immunogène

A 19 amino acid peptide (RILGEEQYNRYQQYGAEEC) corresponding to amino acids 305-323 of the human parkin molecule. An internal peptide sequence was chosen to avoid the possibility of cross reactivity with ubiquitin.
Epitope: a.a. 305-323

Application

Detect Parkin using this Anti-Parkin Antibody, a.a. 305-323 validated for use in ELISA, WB, IH.
Immunohistochemistry: 1:1000 - 1:2000

One site ELISA

Western blot: 1:1000 - 1:2000 (recognizes a doublet at 44-52 kDa on blots of human brain)

The immunogen peptide is available (cat# AG237) for pre-absorbtion controls.

Optimal working dilutions must be determined by the end user.
Research Category
Neuroscience
Research Sub Category
Neurodegenerative Diseases

Forme physique

Rabbit serum. Lyophilized. Reconstitute with 50 μL of sterile distilled water. Centrifuge to remove insoluble material. Contains no preservative.

Stockage et stabilité

Maintain lyophilized material at at -20°C to -70°C for up to 12 months after date of receipt. After reconstitution maintain at -20°C to -70°C in undiluted aliquots for up to 6 months. Avoid repeated freeze/thaw cycles. Glycerol (ACS grade or better) can be added (1:1) for greater stability.

Informations légales

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Clause de non-responsabilité

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

V D'Agata et al.
The European journal of neuroscience, 12(10), 3583-3588 (2000-10-13)
A mutation in the parkin gene has been identified as the cause for an autosomal recessively inherited form of early onset Parkinson's disease. We have recently isolated the mRNA coding for the rat homologue of parkin and showed its widespread
Anna S Gorbunova et al.
Cell death discovery, 9(1), 352-352 (2023-09-26)
Lung cancer is the leading cause of cancer mortality worldwide. In recent years, the incidence of lung cancer subtype lung adenocarcinoma (LUAD) has steadily increased. Mitochondria, as a pivotal site of cell bioenergetics, metabolism, cell signaling, and cell death, are
Nilotinib-induced autophagic changes increase endogenous parkin level and ubiquitination, leading to amyloid clearance.
Lonskaya, I; Hebron, ML; Desforges, NM; Schachter, JB; Moussa, CE
Journal of Molecular Medicine null
Irina Lonskaya et al.
EMBO molecular medicine, 5(8), 1247-1262 (2013-06-06)
Tyrosine kinase inhibitors (TKIs) are effective therapies for leukaemia. Alzheimer is a neurodegenerative disease characterized by accumulation of β-amyloid (plaques) and hyper-phosphorylated Tau (tangles). Here we show that AD animals have high levels of insoluble parkin and decreased parkin-Beclin-1 interaction
Paola Lenzi et al.
International journal of molecular sciences, 22(10) (2021-06-03)
Glioblastoma (GBM) cells feature mitochondrial alterations, which are documented and quantified in the present study, by using ultrastructural morphometry. Mitochondrial impairment, which roughly occurs in half of the organelles, is shown to be related to mTOR overexpression and autophagy suppression.

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