ABS181
Anti-PDE4B2 Antibody
from rabbit, purified by affinity chromatography
Sinónimos:
cAMP-specific 3′,5′-cyclic phosphodiesterase 4B, DPDE4, PDE32
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About This Item
Código UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Productos recomendados
origen biológico
rabbit
Nivel de calidad
forma del anticuerpo
affinity isolated antibody
tipo de anticuerpo
primary antibodies
clon
polyclonal
purificado por
affinity chromatography
reactividad de especies
rat
reactividad de especies (predicha por homología)
human (immunogen homology)
técnicas
western blot: suitable
Nº de acceso NCBI
Nº de acceso UniProt
Condiciones de envío
wet ice
modificación del objetivo postraduccional
unmodified
Información sobre el gen
human ... PDE4B(5142)
Descripción general
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.
Especificidad
This antibody recognizes PDE4B2 at the N-terminus.
Inmunógeno
Epitope: N-terminus
KLH-conjugated linear peptide corresponding to the N-terminus of human PDE4B2.
Aplicación
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
Calidad
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.
Descripción de destino
~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
Forma física
Affinity purified
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
Almacenamiento y estabilidad
Stable for 1 year at 2-8°C from date of receipt.
Nota de análisis
Control
Rat brain membrane tissue lysate
Rat brain membrane tissue lysate
Otras notas
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Cláusula de descargo de responsabilidad
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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Código de clase de almacenamiento
12 - Non Combustible Liquids
Clase de riesgo para el agua (WGK)
WGK 1
Punto de inflamabilidad (°F)
Not applicable
Punto de inflamabilidad (°C)
Not applicable
Certificados de análisis (COA)
Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»
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Encuentre la documentación para los productos que ha comprado recientemente en la Biblioteca de documentos.
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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