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Key Documents

ABS22

Sigma-Aldrich

Anti-PDE4D Antibody

from rabbit

Synonyme(s) :

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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About This Item

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

Source biologique

rabbit

Niveau de qualité

100

Forme d'anticorps

purified antibody

Clone

polyclonal

Espèces réactives

rat, human

Réactivité de l'espèce (prédite par homologie)

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

Technique(s)

western blot: suitable

Numéro d'accès NCBI

NP_001098101

Numéro d'accès UniProt

Q08499

Conditions d'expédition

wet ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... PDE4D(5144)

Description générale

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.

Spécificité

This antibody recognizes PDE4D at the C-terminus.

Immunogène

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

Application

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

Qualité

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.

Description de la cible

~ 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

Forme physique

Format: Purified

Autres remarques

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

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

Sara Marie Katrancha et al.
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
Mi-Hyeon Jeong et al.
JCI insight, 8(13) (2023-07-10)
The mammalian target of rapamycin complex 1 (mTORC1) senses multiple upstream stimuli to orchestrate anabolic and catabolic events that regulate cell growth and metabolism. Hyperactivation of mTORC1 signaling is observed in multiple human diseases; thus, pathways that suppress mTORC1 signaling
Shannon N Leslie et al.
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
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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