ABS181
Anti-PDE4B2 Antibody
from rabbit, purified by affinity chromatography
Sinonimo/i:
cAMP-specific 3′,5′-cyclic phosphodiesterase 4B, DPDE4, PDE32
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About This Item
Codice UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Prodotti consigliati
Origine biologica
rabbit
Livello qualitativo
Forma dell’anticorpo
affinity isolated antibody
Tipo di anticorpo
primary antibodies
Clone
polyclonal
Purificato mediante
affinity chromatography
Reattività contro le specie
rat
Reattività contro le specie (prevista in base all’omologia)
human (immunogen homology)
tecniche
western blot: suitable
N° accesso NCBI
N° accesso UniProt
Condizioni di spedizione
wet ice
modifica post-traduzionali bersaglio
unmodified
Informazioni sul gene
human ... PDE4B(5142)
Descrizione generale
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.
Specificità
This antibody recognizes PDE4B2 at the N-terminus.
Immunogeno
Epitope: N-terminus
KLH-conjugated linear peptide corresponding to the N-terminus of human PDE4B2.
Applicazioni
Anti-PDE4B2 Antibody is an antibody against PDE4B2 for use in WB.
Research Category
Signaling
Signaling
Research Sub Category
GPCR, cAMP/cGMP & Calcium Signaling
GPCR, cAMP/cGMP & Calcium Signaling
Qualità
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.
Western Blot Analysis: 1 µg/mL of this antibody detected PDE4B2 on 10 µg of Rat brain membrane tissue lysate.
Descrizione del bersaglio
~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
Stato fisico
Affinity purified
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
Stoccaggio e stabilità
Stable for 1 year at 2-8°C from date of receipt.
Risultati analitici
Control
Rat brain membrane tissue lysate
Rat brain membrane tissue lysate
Altre note
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Esclusione di responsabilità
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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Codice della classe di stoccaggio
12 - Non Combustible Liquids
Classe di pericolosità dell'acqua (WGK)
WGK 1
Punto d’infiammabilità (°F)
Not applicable
Punto d’infiammabilità (°C)
Not applicable
Certificati d'analisi (COA)
Cerca il Certificati d'analisi (COA) digitando il numero di lotto/batch corrispondente. I numeri di lotto o di batch sono stampati sull'etichetta dei prodotti dopo la parola ‘Lotto’ o ‘Batch’.
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I documenti relativi ai prodotti acquistati recentemente sono disponibili nell’Archivio dei documenti.
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
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.
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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