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Documenti fondamentali

ABS22

Sigma-Aldrich

Anti-PDE4D Antibody

from rabbit

Sinonimo/i:

phosphodiesterase 4D, cAMP-specific, cAMP-specific phosphodiesterase PDE4D6, cAMP-specific 3′,5′-cyclic phosphodiesterase 4D, phosphodiesterase 4D, cAMP-specific (dunce (Drosophila)-homolog phosphodiesterase E3), phosphodiesterase 4D, cAMP-specific (dunc

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100 μG
381,00 €

381,00 €


Spedizione prevista il02 maggio 2025Dettagli


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Cambia visualizzazione
100 μG
381,00 €

About This Item

Codice UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41

381,00 €


Spedizione prevista il02 maggio 2025Dettagli


Richiedi un ordine bulk

Origine biologica

rabbit

Livello qualitativo

Forma dell’anticorpo

purified antibody

Clone

polyclonal

Reattività contro le specie

rat, human

Reattività contro le specie (prevista in base all’omologia)

chimpanzee (based on 100% sequence homology), mouse (based on 90% sequence 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 ... PDE4D(5144)

Descrizione generale

Phosphodiesterase 4D (PDE4D) is a member of the PDE cyclic nucleotides. PDE4D is known to be regulated by protein kinase C (PKC)-Raf-MEK-ERK and also by cAMP in vascular smooth muscle cells. PDE4D is essential to have equilibrium in relaxing and contracting cues to airway smooth muscle. Down-regulation of PDE4D may be associated with analgesic and anti-inflammatory effects. It has also been linked to the risk of stroke, specifically common polygenic stroke.

Specificità

This antibody recognizes PDE4D at the C-terminus.

Immunogeno

GST-tagged recombinant protein corresponding to the C-terminus of human PDE4D.

Applicazioni

Anti-PDE4D Antibody is an antibody against PDE4D for use in WB.

Qualità

Evaluated by Western Blot in rat brain tissue lysate.

Western Blot Analysis: 0.5 µg/mL of this antibody detected PDE4D on 10 µg of rat brain tissue lysate.

Descrizione del bersaglio

~ 59, 68, 85, 90, and 105 kDa observed. UniProtKB/Swiss-Prot Q08499 (PDE4D_HUMAN) entry describes 12 isoforms produced by alternative splicing: Isoform 1 at 91.115 kDa, Isoform 2 at 76.369 kDa, Isoform 3 at 68.607 kDa, Isoform 4 at 66.376 kDa, Isoform 5 at 57.792 kDa, Isoform 6 at 84.428 kDa, Isoform 7 at 23.839 kDa, Isoform 8 at 59.113 kDa, Isoform 9 at 77.705 kDa, Isoform 10 at 76.816 kDa, Isoform 11 at 84.662 kDa, and Isoform 12 at 24.429 kDa

Stato fisico

Format: Purified

Altre note

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

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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Cell reports, 26(10), 2805-2817 (2019-03-07)
Heterozygous coding mutations in TRIO are associated with neurodevelopmental disorders, including autism, schizophrenia, bipolar disorder, and epilepsy, and impair TRIO's biochemical activities. To model mutant alleles, we ablated one or both Trio alleles from excitatory neurons in the cortex and
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Frontiers in aging neuroscience, 12, 576723-576723 (2020-11-17)
Age is the largest risk factor for Alzheimer's disease (AD) and contributes to cognitive impairment in otherwise healthy individuals. Thus, it is critical that we better understand the risk aging presents to vulnerable regions of the brain and carefully design
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Detailed observations of transcriptional, translational and post-translational events in the human brain are essential to improving our understanding of its development, function and vulnerability to disease. Here, we exploited label-free quantitative tandem mass-spectrometry to create an in-depth proteomic survey of
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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

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