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Beta-TrCP (show BTRC Proteins) controls ubiquitination and degradation of liver-enriched transcription factor CREB-H.
Identify a novel pathogenic mutation in CREB3L3 gene in a family with dominant hypertriglyceridemia with a variable pattern of penetrance.
CREBH activated by HBx interacted with HBx protein, leading to a synergistic effect on the expression of AP-1 (show FOSB Proteins) target genes and the proliferation of hepatocellular carcinoma cells and mouse primary hepatocytes.
Taken together, our results demonstrated that human APOA5 (show APOA5 Proteins) is directly regulated by CREBH via CREBHRE and provided a new insight into the role of this liver-specific bZIP transcription factor in lipoprotein metabolism and triglyceride homeostasis
Studies indicate that mutations in CREB3L3 in individuals with extreme hypertriglyceridemia.
a novel mechanism of action of activated CB1R (show CNR1 Proteins) signaling to induce hepatic gluconeogenesis via direct activation of CREBH
Levels of CREB (show CREB1 Proteins) transcripts did NOT significantly differ in the thyroid adenomas and surrounding normal tissues.
analysis of CREB-H trafficking into alternate pathways of ERAD and stress-regulated intramembrane proteolysis
findings show that CREBH an endoplasmic reticulum stress-activated transcription factor, binds to and transactivates the hepcidin (show HAMP Proteins) promoter
key positive regulator of TGF-beta2 (show TGFB2 Proteins) transcription in hepatitis C virus-infected cells
TLR-4 (show TLR4 Proteins) interacts with CREBH to modulate high-density lipoprotein in response to bacterial endotoxin.
CREBH functions as a key metabolic regulator that controls glucose homeostasis across the circadian cycle or under metabolic stress
Ldlr (show LDLR Proteins)(-/-) Creb3l3(-/-) mice developed significantly more atherosclerotic lesions in the aortas than Ldlr (show LDLR Proteins)(-/-) mice.
studies reveal that CREBH functions as a circadian-regulated liver transcriptional regulator that integrates energy metabolism with circadian rhythm.
Very Low Density Lipoprotein (VLDL) assembly and CREBH activation play key roles in the response to hepatic steatosis by up-regulating apoA-IV (show APOA4 Proteins) and promoting assembly and secretion of larger, more triglyceride - enriched VLDL particles.
fasting or glucagon (show GCG Proteins) stimulation modulates lipid homeostasis through acetylation of CREBH.
Overexpression of nuclear CREB3L3 induced systemic lipolysis, hepatic ketogenesis, and insulin (show INS Proteins) sensitivity with increased energy expenditure.
CREBH-Fsp27beta axis is important for regulating lipid droplet dynamics and triglyceride storage in the liver
CREBH activated by HBx interacted with HBx protein, leading to a synergistic effect on the expression of AP-1 (show JUN Proteins) target genes and the proliferation of hepatocellular carcinoma cells and mouse primary hepatocytes.
This gene encodes a member of the basic-leucine zipper family and the AMP-dependent transcription factor family. The encoded protein is localized to the endoplasmic reticulum and acts as a transcription factor activated by cyclic AMP stimulation. The encoded protein binds the cyclic AMP response element (CRE) and the box-B element and has been linked to acute inflammatory response, hepatocellular carcinoma, triglyceride metabolism, and hepcidin expression. Alternative splicing results in multiple transcript variants.
CREB/ATF family transcription factor
, cyclic AMP-responsive element-binding protein 3-like protein 3
, cAMP-responsive element-binding protein 3-like protein 3
, transcription factor CREB-H
, cAMP-responsive element-binding protein 3-like protein 3-A
, cAMP-responsive element-binding protein 3-like protein 3-B
, cyclic AMP-responsive element-binding protein 3-like protein 3-A
, cyclic AMP-responsive element-binding protein 3-like protein 3-B