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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

CAMP responsive element binding protein 3-like 3

CREB-H, CREB3L3, CREB/ATF family transcription factor
CREB3L3 is a liver-specific transcription factor and member of the CREB/ATF transcription factor family (Omori et al., 2001 [PubMed 11353085]).[supplied by OMIM, Apr 2008] (from NCBI)
Top mentioned proteins: CREB, GDNF, LZIP, CAN, OASIS
Papers on CREB-H
Novel CREB3L3 Nonsense Mutation in a Family With Dominant Hypertriglyceridemia.
New
Averna et al., Palermo, Italy. In Arterioscler Thromb Vasc Biol, Dec 2015
OBJECTIVE: Cyclic AMP responsive element-binding protein 3-like 3 (CREB3L3) is a novel candidate gene for dominant hypertriglyceridemia.
Phosphorylation and SCF-mediated degradation regulate CREB-H transcription of metabolic targets.
New
O'Hare et al., London, United Kingdom. In Mol Biol Cell, Sep 2015
We show that this region is subject to multiple phosphorylations, which regulate CREB-H stability by targeting it to the SCF(Fbw1a) E3 ubiquitin ligase.
Hepatic CREB3L3 controls whole-body energy homeostasis and improves obesity and diabetes.
Shimano et al., Tsukuba, Japan. In Endocrinology, 2014
The membrane-bound transcription factor cAMP-responsive element-binding protein 3-like 3 (CREB3L3) has been reported to be activated during fasting and to regulate triglyceride metabolism.
Hypoxia induced downregulation of hepcidin is mediated by platelet derived growth factor BB.
Weiss et al., Innsbruck, Austria. In Gut, 2014
Subsequent experiments were performed in C57BL/6 mice, CREB-H knockout mice, primary hepatocytes and HepG2 cells.
Stimulus-selective induction of the orphan nuclear receptor NGFIB underlies different influences of angiotensin II and potassium on the human adrenal gland zona glomerulosa-specific 3β-HSD isoform gene expression in adrenocortical H295R cells.
Okamura et al., Kyoto, Japan. In Endocr J, 2014
This sharply contrasts with the phosphorylation that occurs in response to both AngII and K(+) on the CREB/ATF family transcription factor ATF2. Chromatin immunoprecipitation assay confirmed that the NGFIB protein occupies the HSD3B1 promoter only after AngII, while ATF2 binds to the CYP11B2 promoter in response to both AngII and K(+).
Gluconeogenic signals regulate iron homeostasis via hepcidin in mice.
Pietrangelo et al., Modena, Italy. In Gastroenterology, 2014
METHODS: We investigated hepatic regulation of Hepcidin expression in C57BL/6Crl, 129S2/SvPas, BALB/c, and Creb3l3-/- null mice.
Varicella-zoster virus glycoprotein expression differentially induces the unfolded protein response in infected cells.
Grose et al., Iowa City, United States. In Front Microbiol, 2013
VZV infection on the other hand upregulated 33 components including a little described stress sensor CREB-H (64-fold) as well as ER membrane components INSIG and gp78, which modulate cholesterol synthesis while downregulating over 20 components mostly associated with ERAD and FOLD.
An orchestrated program regulating secretory pathway genes and cargos by the transmembrane transcription factor CREB-H.
O'Hare et al., London, United Kingdom. In Traffic, 2013
Expression of the CREB3 protein, CREB-H, in 293 cells, upregulated genes involved in secretory capacity, extracellular matrix formation and lipid metabolism and increased secretion of specific cargos.
Multitargeting and antimetastatic potentials of silibinin in human HepG-2 and PLC/PRF/5 hepatoma cells.
Ghavamzadeh et al., Tehrān, Iran. In Nutr Cancer, 2012
Silibinin was capable of suppressing the transcriptional levels of ANGPT2, ATP6L, CAP2, CCR6, CCR7, CLDN-10, cortactin, CXCR4, GLI2, HK2, ID1, KIAA0101, mortalin, PAK1, RHOA, SPINK1, and STMN1 as well as the enzymatic activity of MMP-2 but promoted the transcripts of CREB3L3, DDX3X, and PROX1 in both cells.
The role of CREB-H transcription factor in triglyceride metabolism.
Review
GeneRIF
Lee, Boston, United States. In Curr Opin Lipidol, 2012
Studies indicate that mutations in CREB3L3 in individuals with extreme hypertriglyceridemia.
Excess of rare variants in non-genome-wide association study candidate genes in patients with hypertriglyceridemia.
Hegele et al., London, Canada. In Circ Cardiovasc Genet, 2012
METHODS AND RESULTS: We resequenced protein coding regions of 3 genes with established roles (APOC2, GPIHBP1, LMF1) and 2 genes recently implicated (CREB3L3 and ZHX3) in TG metabolism.
Cannabinoid receptor type 1 (CB1R) signaling regulates hepatic gluconeogenesis via induction of endoplasmic reticulum-bound transcription factor cAMP-responsive element-binding protein H (CREBH) in primary hepatocytes.
GeneRIF
Choi et al., Kwangju, South Korea. In J Biol Chem, 2011
a novel mechanism of action of activated CB1R signaling to induce hepatic gluconeogenesis via direct activation of CREBH
The transcription factor cyclic AMP-responsive element-binding protein H regulates triglyceride metabolism.
Impact
Lee et al., Boston, United States. In Nat Med, 2011
Here we report that the transcription factor cyclic AMP-responsive element-binding protein H (CREB-H, encoded by CREB3L3) is required for the maintenance of normal plasma triglyceride concentrations.
Inhibition of proprotein convertase SKI-1 blocks transcription of key extracellular matrix genes regulating osteoblastic mineralization.
Seidah et al., Kansas City, United States. In J Biol Chem, 2011
Conversely, overexpression of SKI-1-activated SREBP-1a and CREB-H in UMR106-01 osteoblastic cells increased the number of mineralized foci and altered their morphology to yield mineralization nodules, respectively.
N-linked glycosylation is required for optimal proteolytic activation of membrane-bound transcription factor CREB-H.
Jin et al., Hong Kong, Hong Kong. In J Cell Sci, 2010
CREB-H is a liver-enriched bZIP transcription factor of the CREB3 subfamily.
Different mechanisms of recognition and ER retention by transmembrane transcription factors CREB-H and ATF6.
O'Hare et al., Maglie, Italy. In Traffic, 2010
CREB-H and activating transcription factor 6 (ATF6) are transmembrane transcription factors that, in response to endoplasmic reticulum (ER) stress, traffic to the Golgi where they are cleaved by specific proteases, producing the N-terminal domains that effect appropriate transcriptional responses.
ER stress controls iron metabolism through induction of hepcidin.
Impact
GeneRIF
Pietrangelo et al., Modena, Italy. In Science, 2009
findings show that CREBH an endoplasmic reticulum stress-activated transcription factor, binds to and transactivates the hepcidin promoter
Trafficking of the bZIP transmembrane transcription factor CREB-H into alternate pathways of ERAD and stress-regulated intramembrane proteolysis.
GeneRIF
O'Hare et al., Maglie, Italy. In Traffic, 2007
analysis of CREB-H trafficking into alternate pathways of ERAD and stress-regulated intramembrane proteolysis
Expression of cAMP-responsive element binding protein and inducible cAMP early repressor in hyperfunctioning thyroid adenomas.
GeneRIF
Chiovato et al., Florence, Italy. In Eur J Endocrinol, 2002
Levels of CREB transcripts did NOT significantly differ in the thyroid adenomas and surrounding normal tissues.
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