CREB is a beta ZIP transcription factor that activates target genes through cAMP response elements. CREB is able to mediate signals from numerous physiological stimuli, resulting in regulation of a broad array of cellular responses. While CREB is expressed in numerous tissues, it plays a large regulatory role in the nervous system. CREB is believed to play a key role in promoting neuronal survival, precursor proliferation, neurite outgrowth and neuronal differentiation in certain neuronal populations. CREB promotes outgrowth and differentiation as a mediator of Neurotrophin pathways. CREB is able to selectively activate numerous downstream genes through interactions with different dimerization partners. CREB is activated by phosphorylation at Ser133 by various signaling pathways including Erk, Ca2+ and stress signaling.
특이성
Reacts with CREB.
면역원
Recombinant CREB-A protein.
애플리케이션
Anti-CREB Antibody is a Mouse Monoclonal Antibody for detection of CREB also known as cAMP-response Element Binding Protein & has been validated in ELISA & WB.
Research Category Epigenetics & Nuclear Function
Research Sub Category Transcription Factors
Western blot: 1-5 μg/mL. Recognizes the ~43kDa protein.
ELISA: 0.1-1.0 μg/mL
Optimal working dilutions must be determined by end user.
결합
Replaces: 04-218
물리적 형태
Format: Purified
Purified immunoglobulin. Liquid in PBS containing 0.1% sodium azide.
저장 및 안정성
Maintain at 2-8°C in undiluted aliquots for up to 6 months after date of receipt.
분석 메모
Control Jurkat nuclear extract, A-431 whole cell lysate
기타 정보
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
법적 정보
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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 2
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.
The rostral anterior cingulate cortex (rACC) is implicated in processing the emotional component of pain. N-methyl-D-aspartate receptors (NMDARs) are highly expressed in the rACC and mediate pain-related affect by activating a signaling pathway that involves cyclic adenosine monophosphate (cAMP)/protein kinase
The number and subtype composition of N-methyl-d-aspartate receptor (NMDAR) at synapses determines their functional properties and role in learning and memory. Genetically increased or decreased amount of GluN2B affects hippocampus-dependent memory in the adult brain. But in some experimental conditions
Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas, 52(5), e8334-e8334 (2019-05-01)
Studies have shown that an injection with the histamine H4 receptor agonist VUF-8430 modulates emotional memory processes. In the present study, the aim was to verify if intraperitoneal (ip) injection of VUF-8430 (500 ng/kg) in mice affects the synthesis of
Journal of the American Society of Nephrology : JASN, 23(6), 997-1007 (2012-03-24)
Experiments with hyperaldosteronemic animals suggest that, despite lowering plasma aldosterone, salt worsens renal injury by paradoxical activation of the mineralocorticoid receptor (MR). Salt and aldosterone synergistically contribute to renal impairment through Rac1-mediated activation of the MR, but whether angiotensin II
Molecular medicine reports, 11(1), 226-230 (2014-10-24)
Sevoflurane is an inhaled anesthetic that is widely used in clinical practice, particularly for pediatric anesthesia. Previous studies have suggested that sevoflurane may induce neurotoxicity in the brains of neonatal mice. In the present study, the possible mechanism of neurodegeneration