추천 제품
생물학적 소스
rabbit
Quality Level
결합
unconjugated
항체 형태
affinity isolated antibody
항체 생산 유형
primary antibodies
클론
polyclonal
형태
buffered aqueous solution
분자량
~43 kDa
종 반응성
mouse, human, rat
농도
1 mg/mL
기술
immunohistochemistry (formalin-fixed, paraffin-embedded sections): 1:50-1:100
western blot: 1:500-1:1000
동형
IgG
면역원 서열
(R-P-SP-Y-R)
NCBI 수납 번호
UniProt 수납 번호
배송 상태
wet ice
저장 온도
−20°C
타겟 번역 후 변형
phosphorylation (pSer133)
유전자 정보
human ... CREB1(1385)
면역원
Peptide sequence around phosphorylation site of serine 133 (R-P-S(p)-Y-R), according to the protein CREB1.
특징 및 장점
Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.
표적 설명
CREB1 is a transcription factor that is a member of the bZIP family of DNA binding proteins. It binds as a homodimer to the CRE (cAMP-Responsive Element), an octameric palindrome containing a conserved core sequence, 5-prime-TGACG-3-prime. It consists of two transcript variants encoding respective isoforms produced by alternate splicing. It is mapped to 2q32.3-q34 . It is phosphorylated by several protein kinases and induces transcription of genes in response to hormonal stimulation of the cAMP pathway. CREB1 is crucial for the consolidation of long-term conditioned fear memories, but not for encoding, storage, or retrieval of these memories. It is required for the stability of reactivated or retrieved conditioned fear memories .
물리적 형태
Solution in phosphate-buffered saline containing 0.02% sodium azide and 50% glycerol
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
10 - 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.
Viviane de Sousa Tomaz et al.
Journal of affective disorders, 268, 188-200 (2020-03-17)
Depressed patients present increased plasma levels of lipopolysaccharide (LPS) and neuroinflammatory alterations. Here, we determined the neuroimmune effects of different classes of ADs by using the LPS inflammatory model of depression. Male rats received amitriptyline (AMI) a tricyclic, S-citalopram (ESC)
Jing Guo et al.
International journal of clinical and experimental medicine, 7(5), 1297-1306 (2014-07-06)
The mechanisms underlying the pathogenesis of intractable epilepsy (IE) are still unclear. This study aimed to investigate the role of phosphorylation of Cyclase Response Element Binding Protein (p-CREB)/microRNA-132 (miR-132) signal pathway in the epileptogenesis. Temporal lobe epilepsy (TLE) was induced
Seiko Yasuda et al.
Cellular and molecular neurobiology, 34(8), 1199-1208 (2014-08-27)
Depression-like behavior is often complicated by chronic pain. Antidepressants including imipramine (IMI) are widely used to treat chronic pain, but the mechanisms are not fully understood. Brain-derived neurotrophic factor (BDNF) is a neuromodulator that reduces depression by regulating synaptic transmission.
Miaojun Lai et al.
The international journal of neuropsychopharmacology, 17(9), 1397-1407 (2014-05-17)
Inhibition of phosphodiesterase-4 (PDE4), an enzyme that specifically hydrolyzes cyclic adenosine monophosphate (cAMP) increases intracellular cAMP/cAMP-response element binding protein (CREB) signaling. Activation of this signaling is considered as an important compensatory response that decreases motivational properties of drugs of abuse.
Ludmila Gaspar et al.
The European journal of neuroscience, 40(1), 2206-2215 (2014-06-06)
Various lines of evidence suggest a mechanistic role for altered cAMP-CREB (cAMP response element - binding protein) signaling in depressive and affective disorders. However, the establishment and validation of human inter-individual differences in this and other major signaling pathways has
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