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Human CREB1 Protein expressed in Wheat germ - ABIN1350285
Yin, Li, Yang, Gao, Sun, Li: Detection of CREB phosphorylation via Zr (IV) ion mediated signal amplification. in Biosensors & bioelectronics 2014
CREB is positively regulated by PKA and calcium-sensitive calcineurin and negatively by PKC.
The sequence of the CREB gene contains a 88 bp 5' UTR, a 783 bp open reading frame encoding 261 amino acids and a 348 bp 3' UTR.
Data indicate increasing expression for CREB, ATF1, and ATF3 during gastrulation.
findings illustrate the significance of CREB-KDM4B-STAT3 signaling cascade in DNA damage response, and highlight that KDM4B may potentially be a novel oncotarget for colorectal cancer radiotherapy.
CacyBP expression is regulated by E2F1, EGR1, and CREB transcription factors in colorectal cancer HCT116 cells.
ethanol-induced eIF2alpha phosphorylation stimulates COX-2 expression and PGE2 production which induces the BACE1 expression and Abeta production via EP-2 receptor-dependent PKA/CREB pathway.
Creb1/Crtc1-3 and Sec14l3 could be important for early responses of the bronchial epithelium to Th2-stimuli.
CREB1 overexpression rescued the effects on gastric cancer cell growth induced by miR-1297.
Results suggest that low nuclear cyclic AMP responsive element binding protein (pCREB) expression in the primary lesion is significant risk factor for metastatic melanoma.
Via activation of cAMP/PKA/CREB pathway and upregulation of the downstream FtMt expression.
The mechanism of prostaglandin E2-induced transcriptional up-regulation of Oncostatin-M by CREB and Sp1 has been described.
The findings suggest that activation of TGR5 promoted mitochondrial biogenesis in endothelial cells, which is mediated by the CREB/PGC-1a signaling pathway.
High CREB expression is associated with esophageal squamous cell carcinoma.
CREB1 may activate the transcription of wtBRAF through directly binding to its promoter, increasing BRAF expression and regulating the cell proliferation, migration and invasion of endometriosis.
to explore genetic variations in CREB1 promoter region and determine whether these loci affect transcriptional activity and risk on type 2 diabetes (T2D). Three polymorphisms were identified and designated as MU1, MU2 and MU3, respectively. Genotypic distribution analysis revealed that MU1 genotypes presented similar distribution between T2D and healthy controls (P>0.05)
experiments mainly reveal that the CREB1 could affect glucose transport in glioma cells by regulating the expression of GLUT1, which controlled the metabolism of glioma and affected the progression of glioma.
These data highlight a novel arrestin-mediated modulation of CREB signalling, suggesting a reciprocal relationship between arrestin2 and arrestin3, wherein recruitment of arrestin3 restricts the ability of beta2AR to activate prolonged CREB phosphorylation by precluding recruitment of an arrestin2/Src/p38 complex.
The authors conclude that taurodeoxycholic acid-induced DNA damage may depend on the activation of TGR5, CREB and NOX5-S. It is possible that in Barrett's patients bile acids may activate NOX5-S and increase reactive oxygen species (ROS) production via activation of TGR5 and CREB. NOX5-S-derived ROS may cause DNA damage, thereby contributing to the progression from Barrett's esophagus to esophageal adenocarcinoma.
The mechanism of CBP-CREB association via their pKID/KIX domains studied by molecular dynamics free energy simulations has been reported.
Results indicate CREB1 as a critical transcription factor of RRM2 which promotes tumor aggressiveness, and imply a significant correlation between CREB1 and RRM2 in CRC specimens.
Study suggest that both p300 and CREB are required for the function integrity of HIF-1alpha transcription machinery and subsequent angiogenesis, suggesting future studies to improve burn wound healing might be directed to optimization of the interaction between p300, CREB and HIF-1alpha.
These findings suggest that CREB1 may be a potential therapeutic target for the treatment of gastric cancer
YAP/ TAZ pathways contribute to the proliferation/quiescence switch during colon cancer 5FU treatment according to the concerted regulation of Cyclin E1 and CREB
Data show that cAMP-response-element binding protein (CREB) is a central molecular node in the circuit responses after stroke that lead to recovery from motor deficits.
copper chelators regulate the balance between amyloidogenic and nonamyloidogenic processing of AbetaPP via promoting ADAM10 expression through MT1/2 /CREB-dependent signaling pathways.
Storage of passive motion pattern in hippocampal CA1 region depends on CaMKII/CREB signaling pathway in a motion sickness rodent model.
These findings suggest that dendritic region-specific morphological changes in CA1 neurons by constitutive activation of CREB may contribute to improved learning and STM.
this study shows that CREB is a critical regulator of dendritic cells during the germinal center response
FXR exerts its function in L cells through interacting with CREB, a crucial transcriptional regulator of cAMP-CREB signaling pathway, to inhibit its transcriptional activity. Targeting FXR to rescue GLP-1 secretion may be a promising strategy for type II diabetes.
Antioxidative and Anti-Melanogenic Activities of Bamboo Stems (Phyllostachys nigra variety henosis) via PKA/CREB-Mediated MITF Downregulation in B16F10 Melanoma Cells
Unexpectedly, although dispensable for FOXP3 expression and for the homeostasis and suppressive function of thymus-derived Treg cells, CREB negatively regulates the survival of TGF-beta-induced Treg cells, and deletion of CREB resulted in increased FOXP3+ Treg cells in the intestine and protection in a colitis model
The absence of gut microbiota from birth was shown to be associated with decreased CREB expression, followed by decreases of protein kinase C beta (PRKCB) and AMPA receptors expression, and an increase of phosphorylation CREB (pCREB) expression.
Findings suggest that cAMP response element binding protein -mediated hippoacampus structural plasticity is crucial for the role of 5-HT1a receptor in modulating anxiety-related behaviors.
Significant CREB activation in almost the whole amygdala and hippocampus was observed after unconditioned stimulus-retrieval, but conditioned stimulus-retrieval only stimulated CREB activation in the lateral amygdala and the CA3 of hippocampus. In addition, propranolol, a beta-adrenergic receptor antagonist, treatment suppressed memory retrieval-induced CREB activation.
Curc-mPEG454 reverses HFD-induced hepatic steatosis via the activation of CREB inhibition.
Neuron-specific, adult-deletion of CREB1 alters hippocampal structures and causes neuropathological changes resembling aging brain.
analysis of the molecular mechanisms through which CBP stability is regulated by FBXL19 and USP14, which results in the modulation of chromatin remodeling and the expression of cytokine-encoding genes
the requirement of Creb1 for normal mammalian lung morphogenesis is not dependent upon its expression in lung epithelium or mesenchyme, nor its role in musculoskeletal development.
data provide persuasive evidence towards the distinct roles of CREB within the dorsal and ventral hippocampus separately in mediating select nicotine withdrawal phenotypes.
phosphorylation of CREB is downregulated in the Muller glia.
Data suggest that the upregulation of mitochondrial respiratory chain proteins played a partial role in the protection of PKA/CREB signaling.
Both CREB and deltaFosB play a role in the induction of this behavioural sensitization.
Data indicate that Ser738/742-to-glutamate protein kinase D mutant increased AngII-induced CREB protein and activating transcription factor 2 phosphorylation, and phospho-CREB binding to the steroidogenic acute regulatory protein promoter.
SUMO-1 has a role in modifying cAMP-response element-binding protein CREB in prolonged hypoxia.
dsRNA as well as other agonists of endothelial cells elicit signaling mechanisms that include in part CREB phosphorylation mediated by calcium-independent phospholipase A2
the p38-MAPK/CREB pathway plays a critical role in TNFalpha-induced VCAM-1 expression
We found several conserved cis elements in the frog CRF genes including a cAMP response element (CRE), activator protein 1 binding sites, and glucocorticoid response elements
p38 MAPK and CREB function along the dorsal-ventral axis in mesoderm patterning. The phosphorylated form of CREB (S133) is distributed in a gradient along the dorsal-ventral mesoderm axis and the p38 MAPK pathway mediates the phosphorylation of CREB.
modulating CREB activity during early zebrafish development caused significant defects in neural proliferation, midbrain-hindbrain organization and body patterning
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.
cAMP responsive element binding protein 1
, cAMP responsive element binding protein
, cyclic AMP-responsive element-binding protein 1
, active transcription factor CREB
, cAMP-response element-binding protein-1
, cAMP-responsive element-binding protein 1
, transactivator protein
, Y protein
, cAMP response element binding protein 1
, cAMP response element-binding protein
, cyclic AMP-responsive element binding protein, delta
, cyclic AMP-responsive DNA-binding protein