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Key Documents

ABS181

Sigma-Aldrich

Anti-PDE4B2 Antibody

from rabbit, purified by affinity chromatography

Synonyme(s) :

cAMP-specific 3′,5′-cyclic phosphodiesterase 4B, DPDE4, PDE32

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About This Item

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

Source biologique

rabbit

Niveau de qualité

100

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Produit purifié par

affinity chromatography

Espèces réactives

rat

Réactivité de l'espèce (prédite par homologie)

human (immunogen homology)

Technique(s)

western blot: suitable

Numéro d'accès NCBI

NP_001032416

Numéro d'accès UniProt

Q07343

Conditions d'expédition

wet ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... PDE4B(5142)

Catégories apparentées

Description générale

Phosphodiesterase 4B2 (PDE4B2) is a member of the PDE cyclic nucleotides. PDE4B2 is thought to contain both UCR1 and UCR2 regulatory units. PDE4B2 has been associated with schizophrenia and depression and could be a promising target for autism therapies.

Spécificité

This antibody recognizes PDE4B2 at the N-terminus.

Immunogène

Epitope: N-terminus
KLH-conjugated linear peptide corresponding to the N-terminus of human PDE4B2.

Application

Anti-PDE4B2 Antibody is an antibody against PDE4B2 for use in WB.
Research Category
Signaling
Research Sub Category
GPCR, cAMP/cGMP & Calcium Signaling

Qualité

Evaluated by Western Blot in Rat brain membrane tissue lysate.

Western Blot Analysis: 1 µg/mL of this antibody detected PDE4B2 on 10 µg of Rat brain membrane tissue lysate.

Description de la cible

~78 kDa observed. UniProt describes 3 isoforms produced by alternative splicing: Isoform PDE4B1 at 83.3 kDa, Isoform PDE4B2 at 64.5 kDa, and Isoform PDE4B3 at 82.1 kDa

Forme physique

Affinity purified
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Stockage et stabilité

Stable for 1 year at 2-8°C from date of receipt.

Remarque sur l'analyse

Control
Rat brain membrane tissue lysate

Autres remarques

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

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

12 - Non Combustible Liquids

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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Consulter la Bibliothèque de documents

Anthony A Oliva et al.
Journal of neurochemistry, 123(6), 1019-1029 (2012-10-13)
Traumatic brain injury (TBI) results in significant inflammation which contributes to the evolving pathology. Previously, we have demonstrated that cyclic AMP (cAMP), a molecule involved in inflammation, is down-regulated after TBI. To determine the mechanism by which cAMP is down-regulated
Nicole M Wilson et al.
PloS one, 12(5), e0178013-e0178013 (2017-05-26)
Traumatic brain injury (TBI) initiates a deleterious inflammatory response that exacerbates pathology and worsens outcome. This inflammatory response is partially mediated by a reduction in cAMP and a concomitant upregulation of cAMP-hydrolyzing phosphodiesterases (PDEs) acutely after TBI. The PDE4B subfamily
Nicole M Wilson et al.
Frontiers in systems neuroscience, 10, 5-5 (2016-02-24)
Traumatic brain injury (TBI) results in significant impairments in hippocampal synaptic plasticity. A molecule critically involved in hippocampal synaptic plasticity, 3',5'-cyclic adenosine monophosphate, is downregulated in the hippocampus after TBI, but the mechanism that underlies this decrease is unknown. To

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