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.
특이성
This antibody recognizes PDE4B2 at the N-terminus.
면역원
Epitope: N-terminus
KLH-conjugated linear peptide corresponding to the N-terminus of human PDE4B2.
애플리케이션
Anti-PDE4B2 Antibody is an antibody against PDE4B2 for use in WB.
Research Category Signaling
Research Sub Category GPCR, cAMP/cGMP & Calcium Signaling
품질
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.
표적 설명
~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
물리적 형태
Affinity purified
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
저장 및 안정성
Stable for 1 year at 2-8°C from date of receipt.
분석 메모
Control Rat brain membrane tissue lysate
기타 정보
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
면책조항
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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Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 1
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
시험 성적서(COA)
제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.
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
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
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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