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48-602MAG
Buffer Detection Kit for Magnetic Beads
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Detect CREB also known as cAMP-response Element Binding Protein with Anti-CREB Antibody, clone NL904 (Rabbit Monoclonal Antibody), that has been demonstrated to work in IP & WB.
More>>Detect CREB also known as cAMP-response Element Binding Protein with Anti-CREB Antibody, clone NL904 (Rabbit Monoclonal Antibody), that has been demonstrated to work in IP & WB. Less<<
SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
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. Additionally, CREB signaling is involved in learning and memory in several organisms. 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. Some of the kinases involved in phosphorylating CREB at Ser133 are p90RSK, MSK, CaMKIV and MAPKAPK-2.
References
Product Information
Format
Culture Supernatant
HS Code
3002 15 90
Control
Positive Antigen Control: Catalog #12-309, Hela cell nuclear extract. Add an equal volume of Laemmli reducing sample buffer to 10 μL of extract and boil for 5 minutes to reduce the preparation. Load 20 μg of reduced extract per lane for minigels.
Detect CREB also known as cAMP-response Element Binding Protein with Anti-CREB Antibody, clone NL904 (Rabbit Monoclonal Antibody), that has been demonstrated to work in IP & WB.
Key Applications
Immunoprecipitation
Western Blotting
Biological Information
Immunogen
peptide (C-SGAENQQSGDAAVTEAENQQ) corresponding to amino acids 5-24 of human CREB
Epitope
a.a. 5-24
Clone
NL904
Host
Rabbit
Specificity
Recognizes CREB.
Isotype
IgG
Species Reactivity
Human
Mouse
Rat
Species Reactivity Note
Broad species cross-reactivity expected due to sequence homology
This gene encodes a transcription factor that is a member of the leucine zipper family of DNA binding proteins. This protein binds as a homodimer to the cAMP-responsive element, an octameric palindrome. The protein is phosphorylated by several protein kinases, and induces transcription of genes in response to hormonal stimulation of the cAMP pathway. Alternate splicing of this gene results in two transcript variants encoding different isoforms.
FUNCTION: SwissProt: P16220 # This protein binds the cAMP response element (CRE), a sequence present in many viral and cellular promoters. CREB stimulates transcription on binding to the CRE. SIZE: 341 amino acids; 36688 Da SUBUNIT: Binds DNA as a dimer. Interacts PPRC1 and with HTLV-1 Tax-1. SUBCELLULAR LOCATION: Nucleus. PTM: Stimulated by phosphorylation. Phosphorylation of both Ser- 133 and Ser-142 in the SCN regulates the activity of CREB and participates in circadian rhythm generation. Phosphorylation of Ser-133 allows CREBBP and EP300 binding (By similarity). Phosphorylated upon DNA damage, probably by ATM or ATR. SIMILARITY: SwissProt: P16220 ## Belongs to the bZIP family. & Contains 1 bZIP domain. & Contains 1 KID (kinase-inducible) domain.
Molecular Weight
Mr ~43 kDa
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality Assurance
Routinely evaluated by immunoblot on HeLa nuclear extract
Usage Statement
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.
Storage and Shipping Information
Storage Conditions
Stable for 1 year at -20°C from date of receipt. For maximum recovery of product, centrifuge the vial prior to removing the cap. It is suggested product be sub-aliquoted to avoid repeated freeze / thaw cycles.
Inhibition of GPR30 by estriol prevents growth stimulation of triple-negative breast cancer cells by 17β-estradiol. Girgert, R; Emons, G; Gründker, C BMC cancer
14
935
2014
Due to the lack of ERα, triple negative breast cancers (TNBCs) are not susceptible to endocrine therapy using antiestrogens. However, the majority of TNBCs express the membrane bound estrogen receptor GPR30. We have recently shown that knock-down of GPR30 expression prevented growth stimulation of TNBC cell lines by 17β-estradiol. Now we analyzed whether specific inhibition of GPR30 represents a new option for therapy of TNBC.Growth of TNBC cells was assessed using Alamar-blue colorimetric assay. Activation of c-Src and EGF-receptor was assessed using Western blots. Expression of c-fos, cyclin D1 and aromatase was quantified by RT-PCR. Gα-specific signaling of GPR30 was analyzed by electrophoretic mobility shift assay.HCC1806 cells showed the highest GPR30 expression, in HCC70 cells it was clearly lower, in MDA-MB-231 cells it was lowest. 10-8 M 17β-estradiol significantly increased proliferation of HCC1806 cells to 134 ± 12% of control (p less than 0.01). Proliferation of HCC70 cells was slightly increased to 116 ± 8% of control. Estriol significantly reduced cell number of HCC1806 cells to 16 ± 12% (p less than 0.01). Cell number of HCC70 cells and of MDA-MB-231 cells was reduced to 68 ± 25% and to 61 ± 10%, respectively.Activity of Src kinase increased to 150 ± 10% (p less than 0.05) by 10-8 M 17β-estradiol treatment in HCC1806 and to 220 ± 20% in HCC70 cells (p less than 0.01). Estriol treatment completely inhibited 17β-estradiol-induced p-src activation. Transactivation of EGF-receptor increased by estradiol treatment to 350% in HCC1806 and to 280% in HCC70 cells. Estriol completely suppressed EGF-receptor transactivation. c-fos expression increased to 260% and to 190%, respectively. Estriol reduced this induction to 160% (HCC1806) and below control in HCC70 cells. Cyclin D1 was induced to 290% (HCC1806) and 170% (HCC70) and completely inhibited by estriol. 17β-estradiol increased CREB-phosphorylation to 400%. Binding of phospho-CREB to a CRE of cyclin D1 was enhanced to 320%.Specific pharmacological inhibition of GPR30 might become a promising targeted therapy for TNBC in future.
Millipore’s CREB Antibodies demonstrate specificity against CREB, which acts through cAMP response elements. See below for related products for CREB based on the expertise of Upstate & Chemicon. Weitere Informationen >>
