Affinage

CREB3L3

Cyclic AMP-responsive element-binding protein 3-like protein 3 · UniProt Q68CJ9

Length
461 aa
Mass
49.1 kDa
Annotated
2026-06-09
83 papers in source corpus 41 papers cited in narrative 41 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CREB3L3 (CREBH) is a liver- and intestine-enriched, ER-tethered bZIP transcription factor that functions as a master regulator of systemic lipid, glucose, and energy homeostasis across fasting-feeding and circadian cycles (PMID:11353085, PMID:20374965, PMID:27982131, PMID:28461393). Like other CREB3-family factors it is synthesized as a membrane-anchored precursor and activated by regulated intramembrane proteolysis: ER stress or stimulation triggers cleavage by Golgi site-1 and site-2 proteases, liberating an N-terminal fragment that enters the nucleus and binds CRE, box-B, and ATF6 elements to drive transcription (PMID:11353085, PMID:15800215, PMID:16469704). Multiple layers control this activation. ER retention is set by a cytoplasmic ERM determinant rather than lumenal BiP binding as in ATF6, and N-linked glycosylation of three lumenal sites is required for efficient proteolytic activation (PMID:17875199, PMID:19883396, PMID:20356926). GSK-3β/CKII phosphorylation of a serine-rich P-motif both restrains ER-to-Golgi transport by gating COPII association and, in the nuclear product, primes the SDSGIS phosphodegron for SCF(β-TrCP/Fbw1a)-mediated K48 polyubiquitination and proteasomal turnover, while the Sel1L–HRD1 ERAD complex degrades the precursor and active fragment via K294 ubiquitination—coupling transport, stability, and circadian timing through BMAL1 (PMID:27029215, PMID:26108621, PMID:27507854, PMID:28381424, PMID:30389665, PMID:30389664, PMID:33592335). Transcriptional potency is further tuned by PCAF-mediated K294 acetylation and SIRT1 deacetylation, which licenses a CREBH–PPARα heterodimeric complex that binds composite CRE–PPRE elements (PMID:24424044, PMID:26438600). Through this axis CREBH drives the hepatic acute-phase response (CRP, SAP), gluconeogenesis (PEPCK, G6Pase) and glycogenolysis, fatty acid oxidation and ketogenesis, autophagy and lysosomal biogenesis, the mitochondrial unfolded protein response, and an extensive lipoprotein program including ApoA-IV, ApoA-I, FGF21, and intestinal cholesterol handling via Npc1l1 (PMID:16469704, PMID:20374965, PMID:24424044, PMID:24598141, PMID:27982131, PMID:27417587, PMID:27818935, PMID:28461393, PMID:30912978, PMID:39589874). Its secreted C-terminal hepatokine fragment disrupts the ANGPTL3–ANGPTL8 complex to activate lipoprotein lipase and clear triglycerides, and active CREBH additionally normalizes dyslipidemia through an APOE-dependent remodeling of remnant lipoproteins (PMID:36649378, PMID:34491909). Full-length ER-resident CREBH also restrains lipogenesis by sequestering SREBP in the SREBP–INSIG1 complex (PMID:33246135).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 2001 High

    Established CREBH as a liver-specific, ER-membrane-anchored bZIP factor whose activation depends on release from the membrane, defining the basic regulatory logic of a latent transcription factor.

    Evidence GFP imaging, EMSA, GAL4 transactivation and luciferase reporters with transmembrane-domain deletion

    PMID:11353085

    Open questions at the time
    • Did not identify the protease or the physiological activating stimulus
    • DNA-target gene program in vivo not defined
  2. 2006 High

    Identified the activating proteolysis as S1P/S2P cleavage at the Golgi upon ER stress and linked CREBH to the hepatic acute-phase response, converting a localization observation into a defined signaling pathway.

    Evidence In vivo cleavage assay, siRNA knockdown, SAP/CRP promoter reporters, LPS/cytokine challenge in mice

    PMID:16469704

    Open questions at the time
    • How proinflammatory signals are transduced to the cleavage machinery not resolved
    • Did not address ER-retention determinant
  3. 2007 High

    Showed CREBH partitions between ERAD-mediated degradation and the productive cleavage pathway, establishing a stress-tuned switch governing how much active factor is produced.

    Evidence Subcellular fractionation, proteasome inhibition, glycosylation analysis, ERM-deletion mutagenesis

    PMID:17875199

    Open questions at the time
    • E3 ligase mediating basal ERAD not identified at this stage
    • Cellular signals biasing the switch undefined
  4. 2010 High

    Defined the distinct ER-retention mechanism (cytoplasmic ERM, not lumenal BiP) and a glycosylation requirement for activation, separating CREBH mechanistically from ATF6.

    Evidence Domain swap/deletion mutagenesis, BiP co-IP, glycosylation-site mutants with reporter readout

    PMID:19883396 PMID:20356926

    Open questions at the time
    • The trafficking machinery reading the ERM not identified
    • Why glycosylation is required for cleavage mechanistically unresolved
  5. 2010 High

    Connected CREBH to hepatic glucose output via direct binding of gluconeogenic promoters and a PPARα-driven feed-forward induction loop, placing it in fasting metabolic control.

    Evidence ChIP, EMSA, promoter reporters, adenoviral/siRNA manipulation and blood-glucose phenotyping in mice; PPARα PPRE in the CREBH promoter

    PMID:20006574 PMID:20374965

    Open questions at the time
    • Whether glucose effect is fully cell-autonomous in hepatocytes vs systemic not separated
    • Coactivator requirements only partially defined
  6. 2011 High

    Identified upstream inputs and a repressor controlling CREBH activity, showing endocannabinoid/CB1R–JNK signaling induces CREBH and SMILE competes with PGC-1α to dampen it.

    Evidence ChIP, promoter mutagenesis, co-IP/GST pulldown, glucose-production assays in hepatocytes

    PMID:21693703 PMID:21994947

    Open questions at the time
    • Quantitative balance of activators vs SMILE repression in vivo unclear
    • CB1R-to-CREBH signaling steps between JNK and promoter incompletely mapped
  7. 2014 High

    Resolved CREBH–PPARα as a binary complex binding composite CRE–PPRE elements and identified direct apolipoprotein targets, establishing the molecular basis of its lipid/FGF21 transcriptional output.

    Evidence Reciprocal co-IP, ChIP at the FGF21 promoter, EMSA at Apoa4 sites, gain/loss-of-function in mice

    PMID:24424044 PMID:24598141

    Open questions at the time
    • Stoichiometry and structural architecture of the CREBH–PPARα complex unknown
    • Full genome-wide target set not defined
  8. 2015 High

    Defined post-translational tuning of CREBH: PCAF/SIRT1 acetylation at K294 licenses PPARα partnership, while GSK-3/CKII phosphorylation of the P-motif and an SDSGIS phosphodegron target the nuclear form for SCF(β-TrCP/Fbw1a) degradation.

    Evidence Site-directed mutagenesis, co-IP, in vitro kinase assays, ubiquitination assays, in vivo K294R mutant phenotyping

    PMID:26108621 PMID:26438600 PMID:27029215

    Open questions at the time
    • How acetylation and phosphorylation are coordinated on the same molecule unresolved
    • Kinase/acetyltransferase recruitment mechanism not defined
  9. 2016 High

    Integrated CREBH activation into circadian physiology, showing BMAL1/GSK3β-gated COPII-dependent transport rhythmically controls cleavage, and demonstrated genetically separable contributions to fatty acid oxidation/ketogenesis.

    Evidence Circadian cleavage profiling, BMAL1 KO, GSK3β inhibition, COPII co-IP; Creb3l3/Ppara double-KO epistasis

    PMID:27507854 PMID:27982131

    Open questions at the time
    • Direct PPARα-independent target genes for oxidation not fully enumerated
    • Mechanism linking GSK3β phosphorylation to COPII selection incomplete
  10. 2016 High

    Extended CREBH to lipoprotein and cholesterol homeostasis in liver and intestine, directly activating Apoa1 and Fsp27β and repressing intestinal Npc1l1.

    Evidence Reporter assays, reciprocal tissue-specific transgenic and KO mouse models with lipid/atherosclerosis phenotyping

    PMID:25125366 PMID:27417587 PMID:27818935

    Open questions at the time
    • Tissue-specific cofactors distinguishing hepatic vs intestinal programs unclear
    • Fsp27β (lipid storage) vs apolipoprotein (clearance) balance not reconciled
  11. 2017 High

    Mapped additional upstream control (TLR/MyD88–TRAF6 K63-ubiquitination promoting cleavage) and expanded function to circadian glucose homeostasis, fibrogenic TGF-β2, and CYP2B drug metabolism.

    Evidence Co-IP, linkage-specific ubiquitination assays, ChIP, KO mouse phenotyping across inflammatory, glucose, fibrosis and xenobiotic readouts

    PMID:23409047 PMID:27637329 PMID:28461393 PMID:28621467

    Open questions at the time
    • How K63 ubiquitination mechanistically facilitates cleavage unresolved
    • Interplay between inflammatory and metabolic activation inputs not integrated
  12. 2017 High

    Unified P-motif phosphorylation as a dual-purpose control, gating ER-to-Golgi transport of the precursor and the stability of the nuclear product, coupling activation amplitude to nuclear lifetime.

    Evidence GSK-3 inhibition, serine-to-alanine mutagenesis, phosphospecific antibody, fractionation and transcription assays

    PMID:28381424

    Open questions at the time
    • Spatial separation of the two P-motif functions not fully resolved
    • Phosphatase counter-regulation unknown
  13. 2018 High

    Identified the Sel1L–HRD1 ERAD complex as the dominant E3 system controlling CREBH abundance via K294 K48-ubiquitination, with FGF21 as a key output, defining a stress/feeding-tuned protein-stability rheostat.

    Evidence Liver-specific Sel1L and HRD1 KO mice, K294 ubiquitin site-mapping, co-IP, stability assays, FGF21 measurement (two groups)

    PMID:30389664 PMID:30389665

    Open questions at the time
    • Relationship between K294 ubiquitination and K294 acetylation on the same residue not mechanistically reconciled
    • How ERAD selects CREBH among substrates unclear
  14. 2019 High

    Established CREBH as a transcriptional driver of hepatic autophagy and lysosomal biogenesis acting with PPARα/PGC-1α, broadening its catabolic role beyond gene-by-gene metabolic targets.

    Evidence KO mouse autophagy-flux phenotyping, co-IP of the CREBH–PPARα–PGC-1α complex, ChIP on autophagy gene promoters

    PMID:30912978

    Open questions at the time
    • Direct vs indirect regulation of individual ATG genes not fully separated
    • Coordination with mTOR/TFEB autophagy control unknown
  15. 2020 Medium

    Revealed a non-transcriptional ER function: full-length CREBH retains SREBP via the SREBP–INSIG1 complex, positioning CREBH as a brake on lipogenesis in addition to its nuclear catabolic program.

    Evidence Co-IP, SREBP nuclear/cytoplasmic fractionation, KO and tissue-specific KO lipid phenotyping; glycosylation modulation of activation

    PMID:32996649 PMID:33246135

    Open questions at the time
    • Single-lab interaction data awaits independent replication
    • Whether precursor sequestration competes quantitatively with cleavage in vivo unresolved
  16. 2021 High

    Demonstrated mechanistic specificity in triglyceride clearance: CREBH normalizes diabetic dyslipidemia through APOE-dependent remnant clearance (LPL-independent), and circadian HRD1/Sel1L turnover of CREBH shapes diurnal lipid/glucose profiles.

    Evidence LPL-deficient and Apoe-/- genetic epistasis with CREBH adenovirus; HRD1/CREBH KO circadian metabolite profiling with rescue

    PMID:33592335 PMID:34491909

    Open questions at the time
    • How CREBH alters APOE/APOC3 ratios on particles mechanistically unclear
    • Reconciliation of LPL-dependent (hepatokine) and LPL-independent (APOE) clearance routes incomplete
  17. 2023 High

    Identified the secreted C-terminal hepatokine CREBH-C as an endocrine effector, showing CaMKII-dependent secretion and disruption of the ANGPTL3–ANGPTL8 complex to activate LPL, giving the C-terminal fragment its own signaling function.

    Evidence Conditioned-media/plasma detection, CaMKII inhibition/kinase assay, ANGPTL3–ANGPTL8 co-IP, in vivo LPL activity and CREBH-C administration

    PMID:36649378

    Open questions at the time
    • Receptor or surface engagement of CREBH-C at peripheral tissues unknown
    • Relative contribution of CREBH-C vs nuclear CREBH to lipid lowering not quantified
  18. 2024 High

    Linked CREBH to mitochondrial proteostasis and contact-site biology, showing it expands MAMs and, with PPARα, drives the UPRmt regulators ATF5/ATF4 to sustain fatty acid oxidation.

    Evidence MAM fractionation, KO mouse phenotyping, membrane-potential and unfolded-protein assays, co-IP, metabolic flux

    PMID:39589874

    Open questions at the time
    • Mechanism by which CREBH promotes MAM expansion not defined
    • Direct ChIP evidence at ATF5/ATF4 loci not detailed
  19. 2025 Medium

    Expanded the inter-organ output of CREBH, identifying secreted hepatokine Cgref1 as a mediator of adipose insulin resistance and confirming conserved intestinal lipid-flux control in zebrafish.

    Evidence Creb3l3-/- multi-omics and Cgref1 KO mice; zebrafish creb3l3 double mutants with lipoprotein reporters and lipid-droplet analysis

    PMID:40303310 PMID:40449732

    Open questions at the time
    • Direct ChIP confirmation of CREBH binding at the Cgref1 promoter lacking
    • Whether intestinal mechanism in fish fully translates to mammalian enterocytes untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the competing fates of CREBH—ERAD degradation, productive RIP cleavage, SREBP sequestration, and C-terminal hepatokine secretion—are quantitatively coordinated by a single stress/feeding/circadian input remains unresolved.
  • No integrated model partitioning precursor flux among ERAD, cleavage, and SREBP retention
  • Structural basis of CREBH–PPARα complex and its acetylation-dependent assembly unknown
  • Receptors for secreted CREBH-C and Cgref1 unidentified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 6 GO:0003677 DNA binding 3 GO:0140313 molecular sequestering activity 2
Localization
GO:0005634 nucleus 4 GO:0005783 endoplasmic reticulum 4 GO:0005794 Golgi apparatus 3 GO:0005576 extracellular region 1 GO:0005739 mitochondrion 1
Pathway
R-HSA-1430728 Metabolism 6 R-HSA-392499 Metabolism of proteins 5 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-8953897 Cellular responses to stimuli 3 R-HSA-9909396 Circadian clock 3 R-HSA-168256 Immune System 2 R-HSA-9612973 Autophagy 2
Partners
BTRC (Β-TRCP/FBW1A)CREBZF (SMILE)HRD1 (SYVN1)INSIG1PPARASEL1LSREBF (SREBP)TRAF6
Complex memberships
CREBH–PPARα transcriptional complexSCF(β-TrCP/Fbw1a) E3 ligase complex (substrate)SREBP–INSIG1 complex (associated)Sel1L–HRD1 ERAD complex (substrate)

Evidence

Reading pass · 41 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 CREB-H (CREBH) is a liver-specific bZIP transcription factor localized to the ER via a transmembrane domain; deletion of the transmembrane domain causes nuclear translocation and increases transcriptional activity. Full-length GFP-CREBH localizes to perinuclear reticular structures, while the TM-deleted mutant localizes to the nucleus. CREBH binds CRE and box-B elements but not C/EBP, AP-1, or NF-κB elements. GFP fusion live imaging, gel mobility shift assay, GAL4 fusion transactivation assay, luciferase reporter assay Nucleic acids research High 11353085
2005 CREB-H is activated by proteolytic cleavage that removes the C-terminal transmembrane domain, releasing a nuclear fragment. The active form binds to CRE, box-B, and ATF6-binding elements and activates the PEPCK-C promoter; this activation is further stimulated by cAMP and protein kinase A. Luciferase reporter assay, co-immunoprecipitation, promoter activation assay, cell proliferation assay Nucleic acids research Medium 15800215
2006 Upon ER stress, CREBH is cleaved by site-1 protease (S1P) and site-2 protease (S2P) at the Golgi to liberate an N-terminal fragment that translocates to the nucleus and activates transcription of acute phase response genes SAP and CRP. Proinflammatory cytokines (and LPS) induce CREBH expression and trigger its cleavage in vivo. In vivo cleavage assay, siRNA knockdown, promoter-luciferase reporter, mouse LPS/cytokine challenge Cell High 16469704
2007 CREB-H is subject to N-linked glycosylation and undergoes ERAD: it is retrotranslocated from the ER to the cytosol, deglycosylated, and degraded by the proteasome under basal conditions. Proteasome inhibition diverts CREB-H from ERAD into the cleavage/nuclear-transport pathway. A cytoplasmic determinant (ERM) mediates ER retention; deletion of this motif causes constitutive Golgi localization and cleavage. Subcellular fractionation, proteasome inhibitor treatment, glycosylation analysis, deletion mutagenesis, nuclear transport assay Traffic (Copenhagen, Denmark) High 17875199
2009 PPARα directly binds to a PPRE in the CREBH promoter to induce CREBH expression in response to fatty acids and fasting. CREBH mRNA and nuclear protein are induced by fasting and suppressed by refeeding; this suppression is impaired in ob/ob mice. Luciferase reporter assay, EMSA, ChIP assay, promoter deletion analysis, PPARα agonist/antagonist treatment Biochemical and biophysical research communications High 20006574
2010 Unlike ATF6, whose ER retention is mediated by lumenal BiP binding, CREB-H ER retention is controlled by a membrane-proximal cytoplasmic determinant (ERM) conserved in the CREB3 family but absent in ATF6. The lumenal tail of CREB-H neither binds BiP nor is required for ER retention or Golgi transport; ERM deletion causes constitutive Golgi localization and cleavage by S1P. Domain deletion and swap mutagenesis, co-IP for BiP binding, fluorescence microscopy, constitutive cleavage assay Traffic (Copenhagen, Denmark) High 19883396
2010 N-linked glycosylation of CREB-H at three luminal sites is required for its efficient proteolytic activation. Unglycosylated CREB-H mutant (all three N-glycosylation sites abolished) is retained in an inactive ER form and fails to be cleaved or activate transcription in response to S1P stimulation. Site-directed mutagenesis of glycosylation sites, brefeldin A / KDEL-S1P stimulation, transcription reporter assay Journal of cell science High 20356926
2010 CREBH regulates hepatic gluconeogenesis: it is induced by fasting or insulin-resistant state in a dexamethasone- and PGC-1α-dependent manner; the active nuclear form (CREBH-N) binds an enhancer in the PEPCK-C and G6Pase promoters distinct from the classical CREB/CRTC2 sites; hepatic CREBH knockdown reduces blood glucose in mice. Adenoviral overexpression, siRNA knockdown, ChIP assay, promoter-luciferase, glucose tolerance/blood glucose measurement in mice Cell metabolism High 20374965
2011 CB1R activation by 2-AG induces CREBH gene expression via JNK phosphorylation and c-Jun binding to an AP-1 site in the CREBH promoter. CREBH mediates CB1R-stimulated hepatic gluconeogenic gene expression and glucose production; endogenous CREBH knockdown abolishes 2-AG-induced gluconeogenesis. ChIP assay, promoter mutagenesis-luciferase, siRNA knockdown, glucose production assay in primary hepatocytes The Journal of biological chemistry High 21693703
2011 SMILE (small heterodimer partner-interacting leucine zipper protein) interacts with CREBH via its bZIP domain and represses CREBH-mediated transactivation. SMILE competes with PGC-1α coactivation of CREBH; curcumin induces SMILE through LKB1/AMPK signaling to selectively inhibit CREBH (not ATF6) target gene transcription. Co-IP, GST pulldown, ChIP, Gal4 fusion transactivation, siRNA knockdown, dominant-negative assay The Journal of biological chemistry High 21994947
2012 CB1R agonist 2-AG induces Lipin1 gene expression in a CREBH-dependent manner; CREBH directly recruits to the Lipin1 promoter. This increases hepatic diacylglycerol levels and PKCε phosphorylation, thereby inhibiting insulin receptor signaling. ChIP assay, adenoviral CREBH overexpression/knockdown, DAG measurement, PKCε phosphorylation assay, insulin receptor signaling assay The Journal of biological chemistry Medium 22989885
2013 CREB-H contains a unique ATB domain (absent in all other human bZIP factors) essential for transcriptional activity. CREB-H activates secretory pathway genes (SPGs) and stimulates secretion of specific cargo including apolipoproteins (ApoA-IV, ApoAI) in liver cells. Drosophila ATB domain complementation, deletion mutagenesis, transcriptomics, ELISA for secreted proteins Traffic (Copenhagen, Denmark) Medium 23279168
2014 CREBH and PPARα interact to form a functional binary transcriptional complex that binds integrated CRE–PPRE composite elements in the FGF21 promoter; PPARα requires CREBH to exert its trans-activation effect on FGF21. CREBH and PPARα mutually regulate each other's expression. Co-IP, ChIP, luciferase reporter, gain- and loss-of-function in mice (adenoviral and genetic), FGF21 protein measurement Endocrinology High 24424044
2014 CREBH directly activates Apoa4 (apolipoprotein A-IV) transcription via two tandem CREBH-binding sites (5'-CCACGTTG-3') in the promoter conserved between human and mouse; CREBH protein is constitutively processed to its active form in normal liver, with further increase during steatosis. ChIP, EMSA, luciferase reporter, CREBH-deficient mouse transcriptomics Journal of lipid research High 24598141
2015 CREBH is acetylated at lysine 294 (K294) within its bZIP domain during fasting. PCAF mediates acetylation, SIRT1 mediates deacetylation. K294 acetylation is required for CREBH–PPARα interaction and synergistic transcriptional activation of lipid metabolic target genes; acetylation-deficient (K294R) mutant abolishes this interaction and causes hepatic steatosis in vivo. Site-directed mutagenesis, co-IP, luciferase reporter, adenoviral K294 mutant injection into mice, hepatic lipid measurement Molecular and cellular biology High 26438600
2015 CREBH directly activates the Fsp27β (liver-specific isoform) promoter (not the Fsp27α/PPARγ-driven promoter). Fsp27β localizes to lipid droplets and suppresses lipolysis; CREBH-driven Fsp27β expression promotes lipid droplet enlargement and triglyceride accumulation in the liver. Promoter-luciferase assay, adenoviral overexpression/KO mouse, Oil-Red-O staining, lipid droplet imaging Hepatology (Baltimore, Md.) Medium 25125366
2015 The active nuclear form of CREB-H (CREB-H-ΔTC) is degraded by the SCF(β-TrCP) E3 ubiquitin ligase via K48-linked polyubiquitination. β-TrCP binds a conserved phosphodegron motif SDSGIS in CREB-H-ΔTC; phosphorylation of this motif is required for β-TrCP recognition and subsequent proteasomal degradation. Co-IP, ubiquitination assay, site-directed mutagenesis, siRNA knockdown of β-TrCP, cycloheximide chase Scientific reports High 27029215
2015 Phosphorylation of CREB-H within a serine-rich P-motif (around S87/S90) by CKII and GSK-3β targets CREB-H to the SCF(Fbw1a/β-TrCP) E3 ligase for proteasomal degradation. CREB-H directly interacts with Fbw1a in a phosphorylation-dependent manner; GSK-3 phosphorylation at adjacent serines primes subsequent CKII phosphorylation at S87/S90. In vitro kinase assay with CKII and GSK-3β, phosphospecific antibody, dominant-negative Cul1, Co-IP, site-directed mutagenesis Molecular biology of the cell High 26108621
2016 CREBH proteolytic activation exhibits circadian rhythmicity controlled by the core clock oscillator BMAL1 and AKT/GSK3β signaling. GSK3β-mediated phosphorylation of CREBH modulates its association with COPII vesicle components to control ER-to-Golgi transport and subsequent proteolytic cleavage in a circadian manner. Circadian profiling of CREBH cleavage in mouse livers, BMAL1 KO, GSK3β inhibitor, COPII co-IP, phosphorylation assay Diabetes High 27507854
2016 Hepatic CREB3L3 independently controls fatty acid oxidation and ketogenesis in addition to its role in activating PPARα in an auto-loop; double knockout (Creb3l3-/-/Ppara-/-) mice show further suppression of oxidation/ketogenesis genes beyond either single KO, indicating independent contributions. Creb3l3-/- and Ppara-/- single and double knockout mouse phenotyping on ketogenic diet and fasting; gene expression analysis Scientific reports High 27982131
2016 CREBH directly activates Apoa1 (apoA-I) gene transcription, contributing to HDL cholesterol production. CREBH deficiency in Ldlr-/- mice decreases HDL and apoA-I and accelerates atherosclerosis. Luciferase reporter assay, CREBH-deficient/Ldlr-/- double KO mouse phenotyping, lipid profiling Arteriosclerosis, thrombosis, and vascular biology Medium 27417587
2016 Intestinal CREBH directly regulates Npc1l1 (cholesterol transporter) promoter activity to suppress intestinal cholesterol absorption; CREBH transgenic (intestine) mice show reduced Npc1l1 expression and decreased plasma/hepatic cholesterol, while CREBH null mice show the opposite. Promoter-luciferase assay, CREBH intestine-specific transgenic and global KO mice, cholesterol absorption measurement, fecal cholesterol output Molecular metabolism High 27818935
2017 CREBH maintains circadian glucose homeostasis by regulating glycogenolysis (via PYGL) and gluconeogenesis (via PCK1 and G6PC). CREBH interacts with PPARα, and K294 acetylation controls this interaction and synergistic gluconeogenic activity across the circadian cycle. CREBH KO mouse circadian phenotyping, Co-IP, adenoviral K294 acetylation-site mutants, glycogen measurement, blood glucose profiling Molecular and cellular biology High 28461393
2017 TLR/MyD88-dependent signaling activates CREBH in liver upon LPS. TRAF6 (E3 ubiquitin ligase, TLR mediator) interacts with CREBH in a MyD88-dependent manner and mediates K63-linked ubiquitination of CREBH to facilitate its cleavage and activation. Active CREBH then directly activates ApoA4 expression to modulate HDL. Co-IP (CREBH–TRAF6, CREBH–MyD88), K63-ubiquitination assay, ChIP on ApoA4 promoter, TLR/MyD88 KO mice, HDL measurement The Journal of biological chemistry High 27637329
2017 CREBH directly binds CREBH-recognition sites in the TGF-β2 promoter to induce TGF-β2 transcription in HCV-infected hepatocytes. Active nuclear CREBH accumulates during HCV infection, and CREBH silencing reduces TGF-β2 expression and fibrogenic responses in hepatic stellate cells. EMSA, ChIP, promoter-luciferase, siRNA knockdown, CREBH null mouse model, co-culture of HCV-infected cells with HSCs Hepatology (Baltimore, Md.) High 28621467
2017 GSK-3 phosphorylation of the P-motif (S73–S90) of the full-length CREB-H precursor promotes ER retention and prevents ER-to-Golgi transport; mutation of these serines or pharmacological GSK-3 inhibition causes constitutive Golgi transport, proteolytic cleavage, and nuclear import. The same P-motif in the nuclear product is also phosphorylated by GSK-3/CKII to target CREB-H for SCF-mediated degradation, providing integrated control coupling ER-to-Golgi transport with nuclear stability. GSK-3 inhibitor treatment, serine-to-alanine mutagenesis, phosphospecific antibody, immunofluorescence, nuclear fractionation, transcriptional assay Molecular biology of the cell High 28381424
2018 The Sel1L–HRD1 ERAD complex regulates ubiquitination and proteasomal turnover (and thus nuclear abundance) of CREBH in the liver. Liver-specific Sel1L deletion elevates CREBH nuclear levels and dramatically increases FGF21 expression; this is specifically through CREBH (not PPARα). An inverse correlation between Sel1L–HRD1 ERAD activity and CREBH–FGF21 levels was demonstrated across fasting-feeding cycles. Liver-specific Sel1L KO mice, ubiquitination assay, Co-IP, FGF21 measurement, CREBH protein stability assay The EMBO journal High 30389665
2018 HRD1 E3 ligase mediates K48-linked polyubiquitin conjugation onto CREBH at lysine 294 (K294) for proteasomal degradation to downregulate FGF21 expression. Liver-specific HRD1 deletion phenocopies FGF21 gain-of-function mice (growth retardation, female infertility, circadian disruption). Liver-specific HRD1 KO mice, ubiquitin site-mapping at K294, ubiquitination assay, FGF21/CREBH protein turnover assay The EMBO journal High 30389664
2019 CREBH activates expression of key autophagy genes (LC3, ATG7, ATG2b, ULK1) and lysosomal biogenesis genes in the liver upon starvation or energy-demanding circadian phases. CREBH deficiency reduces hepatic autophagic activity and increases lipid accumulation upon starvation. Under starvation, CREBH interacts with PPARα and PGC-1α to synergistically drive autophagy gene expression. CREBH KO mouse phenotyping, autophagy flux assay, Co-IP (CREBH–PPARα–PGC-1α), ChIP, gene expression analysis, adenoviral CREBH overexpression FASEB journal High 30912978
2020 N-glycosylation of CREBH enhances its proteolytic activation and transcriptional capacity. N-glycosylation modulates CREBH's ability to activate PPARα and SCD-1 promoters via protein interactions. Deglycosylated CREBH shows impaired proteolysis (PA-induced cleavage blocked by tunicamycin), increased lipogenesis, and lipotoxicity in cells and NAFLD mouse models. Glycosylation site mutagenesis, GnT-V hyperglycosylation, tunicamycin treatment, Co-IP (CREBH–PPARα, CREBH–SCD-1), promoter-luciferase, lentivirus injection mouse model FASEB journal Medium 32996649
2020 Full-length CREBH in the ER physically interacts with SREBP proteins and promotes formation of the SREBP-INSIG1 complex, retaining SREBP in the ER and preventing its proteolytic activation at the Golgi. CREBH deficiency leads to accumulation of nuclear SREBP, thereby de-repressing lipogenic/cholesterogenic gene expression. Co-IP (CREBH–SREBP–INSIG1), nuclear/cytoplasmic fractionation of SREBP, CREBH KO and liver/intestine-specific KO mouse lipid phenotyping Cellular and molecular gastroenterology and hepatology Medium 33246135
2021 The HRD1/Sel1L ERAD complex mediates circadian polyubiquitination and degradation of CREBH protein across the circadian cycle; HRD1 and Sel1L expression itself is rhythmically driven by CREBH–PPARα–BMAL1. HRD1 liver-specific KO increases CREBH levels, altering circadian TG, FA, and glucose profiles; suppressing CREBH overproduction in HRD1 LKO mice rescues diurnal lipid profiles. Liver-specific HRD1 KO and CREBH KO mice, circadian metabolite profiling, ubiquitination assay, Co-IP (CREBH–PPARα–BMAL1), rescue by CREBH suppression in HRD1 LKO Molecular metabolism High 33592335
2023 The C-terminal fragment of CREBH (CREBH-C), derived from cleavage of full-length CREBH, is secreted as a hepatokine in response to fasting or hepatic stress. CaMKII-mediated phosphorylation of CREBH-C is required for its efficient secretion via exocytosis. Secreted CREBH-C blocks formation of the ANGPTL3–ANGPTL8 inhibitory complex, thereby increasing LPL activity in plasma and metabolic tissues, promoting triglyceride clearance. CREBH-C detection in conditioned media and plasma, CaMKII inhibitor and kinase assay, ANGPTL3–ANGPTL8 Co-IP in presence of CREBH-C, LPL activity assay in vivo, CREBH-C administration to high-fat diet mice Science signaling High 36649378
2021 CREBH normalizes diabetic dyslipidemia via an APOE-dependent mechanism: active CREBH enriches APOE on TRL remnants and depletes APOC3, promoting hepatic clearance of remnant lipoproteins. This mechanism is independent of LPL (confirmed in LPL-deficient mice) but requires APOE (fails in Apoe-/- mice). LPL-deficient and Apoe-/- mouse genetic models with CREBH adenoviral expression, lipoprotein particle profiling, apolipoprotein composition analysis The Journal of clinical investigation High 34491909
2022 CREBH promotes SIRT3 expression, which deacetylates MnSOD to reduce mitochondrial oxidative stress and inhibits NLRP3 inflammasome activation. CREBH overexpression alleviates mitochondrial oxidative stress in NASH; SIRT3 suppression abolishes this protective effect; CREBH KO mice show elevated oxidative stress and NASH susceptibility. Co-IP (SIRT3–CPT2, SIRT3–ACADL interaction), acetylation assay of MnSOD, NLRP3 inflammasome activation measurement, CREBH KO and OE mouse/cell models Free radical biology & medicine Medium 35926687
2024 CREBH is enriched in and required for hepatic Mitochondria-Associated Membrane (MAM) expansion under energy demands. Activated CREBH, cooperating with PPARα, drives expression of UPRmt regulators ATF5 and ATF4. CREBH deficiency causes accumulation of mitochondrial unfolded proteins, decreased mitochondrial membrane potential, and shifts energy metabolism from fatty acid oxidation toward carbohydrate oxidation. MAM fractionation, CREBH KO mouse phenotyping, mitochondrial membrane potential assay, mitochondrial unfolded protein detection, Co-IP (CREBH–PPARα), gene expression analysis, metabolic flux measurement Proceedings of the National Academy of Sciences High 39589874
2015 TNFα induces CREBH expression via NF-κB signaling in osteoblasts; active CREBH increases Smurf1 expression leading to ubiquitin-dependent degradation of Smad1, thereby inhibiting BMP2-induced osteoblast differentiation. CREBH knockdown attenuates TNFα-mediated Smad1 degradation and rescues osteoblast differentiation. Co-IP (Smad1–Smurf1), siRNA knockdown, adenoviral CREBH overexpression, ALP/osteocalcin assays, ectopic bone formation in vivo The Journal of biological chemistry Medium 25873397
2013 Hepatic CREBH is a positive transcriptional regulator of CYP2B family genes (e.g., CYP2B10); CREBH ectopic expression increases CYP2B10 promoter activity, and CREBH-deficient mice show severely impaired CYP2B induction and resistance to sulpyrine-induced fatal shock. Reintroduction of CYP2B into CREBH-deficient liver restores sulpyrine susceptibility. Promoter-luciferase assay, CREBH KO mouse, in vivo knockdown (siRNA), adenoviral CYP2B rescue PloS one Medium 23409047
2025 CREB-H induces expression of Cgref1 (a secreted hepatokine) via direct transcriptional regulation. Secreted Cgref1 suppresses insulin signaling and glucose uptake in epididymal white adipose tissue, creating eWAT insulin resistance that in turn promotes hepatic de novo lipogenesis. Microarray of Creb3l3-/- mice, Cgref1 KO mice, transcriptomic/metabolomic/lipidomic analysis, gain/loss-of-function in hepatocytes, insulin signaling assay in eWAT International journal of biological sciences Medium 40303310
2025 In zebrafish creb3l3 double mutants (lacking both orthologs), key creb3l3 target genes apoC2 and apoA4 are downregulated in intestines; mutants show impaired lipoprotein turnover (not reduced total lipoprotein production) and increased enterocyte lipid droplet size and number, establishing creb3l3 as a regulator of postprandial intestinal lipid flux balancing storage vs. secretion. Zebrafish genetic KO (CRISPR), lipoprotein reporter lines, histological lipid droplet analysis, gene expression analysis Journal of lipid research Medium 40449732
2023 CREBH promotes autophagic flux by transcriptionally repressing Coronin 1a (Coro1a), a gene that inhibits autophagosome-lysosome fusion. Overexpression of Coro1a in hepatocytes blocks autophagic flux; CREBH deficiency aggravates dysfunctional autophagy and liver injury in NASH. Autophagic flux assay (LC3-II, p62), lysosomal marker (LAMP1) imaging, CREBH KO in NASH mouse models, Coro1a promoter reporter, adenoviral Coro1a overexpression Biochimica et biophysica acta. Molecular basis of disease Medium 37837948

Source papers

Stage 0 corpus · 83 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Endoplasmic reticulum stress activates cleavage of CREBH to induce a systemic inflammatory response. Cell 669 16469704
2010 Regulation of hepatic gluconeogenesis by an ER-bound transcription factor, CREBH. Cell metabolism 158 20374965
2001 CREB-H: a novel mammalian transcription factor belonging to the CREB/ATF family and functioning via the box-B element with a liver-specific expression. Nucleic acids research 137 11353085
2014 Liver-enriched transcription factor CREBH interacts with peroxisome proliferator-activated receptor α to regulate metabolic hormone FGF21. Endocrinology 115 24424044
2015 Transcriptional activation of Fsp27 by the liver-enriched transcription factor CREBH promotes lipid droplet growth and hepatic steatosis. Hepatology (Baltimore, Md.) 90 25125366
2005 The liver-enriched transcription factor CREB-H is a growth suppressor protein underexpressed in hepatocellular carcinoma. Nucleic acids research 85 15800215
2018 Hepatic Sel1L-Hrd1 ER-associated degradation (ERAD) manages FGF21 levels and systemic metabolism via CREBH. The EMBO journal 80 30389665
2023 Akkermansia muciniphila and its membrane protein ameliorates intestinal inflammatory stress and promotes epithelial wound healing via CREBH and miR-143/145. Journal of biomedical science 75 37287024
2018 CREBH Regulates Systemic Glucose and Lipid Metabolism. International journal of molecular sciences 69 29738435
2016 CREBH Couples Circadian Clock With Hepatic Lipid Metabolism. Diabetes 68 27507854
2009 The liver-enriched transcription factor CREBH is nutritionally regulated and activated by fatty acids and PPARalpha. Biochemical and biophysical research communications 63 20006574
2018 HRD1-ERAD controls production of the hepatokine FGF21 through CREBH polyubiquitination. The EMBO journal 59 30389664
2014 Hepatic CREB3L3 controls whole-body energy homeostasis and improves obesity and diabetes. Endocrinology 57 25233440
2011 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. The Journal of biological chemistry 54 21693703
2017 CREBH Maintains Circadian Glucose Homeostasis by Regulating Hepatic Glycogenolysis and Gluconeogenesis. Molecular and cellular biology 50 28461393
2016 CREB3L3 controls fatty acid oxidation and ketogenesis in synergy with PPARα. Scientific reports 48 27982131
2015 Lysine Acetylation of CREBH Regulates Fasting-Induced Hepatic Lipid Metabolism. Molecular and cellular biology 47 26438600
2014 Transcriptional regulation of apolipoprotein A-IV by the transcription factor CREBH. Journal of lipid research 42 24598141
2013 An orchestrated program regulating secretory pathway genes and cargos by the transmembrane transcription factor CREB-H. Traffic (Copenhagen, Denmark) 42 23279168
2011 Curcumin differentially regulates endoplasmic reticulum stress through transcriptional corepressor SMILE (small heterodimer partner-interacting leucine zipper protein)-mediated inhibition of CREBH (cAMP responsive element-binding protein H). The Journal of biological chemistry 41 21994947
2018 Dietary protein restriction reduces circulating VLDL triglyceride levels via CREBH-APOA5-dependent and -independent mechanisms. JCI insight 39 30385734
2016 Intestinal CREBH overexpression prevents high-cholesterol diet-induced hypercholesterolemia by reducing Npc1l1 expression. Molecular metabolism 37 27818935
2012 Pretreatment with CO-releasing molecules suppresses hepcidin expression during inflammation and endoplasmic reticulum stress through inhibition of the STAT3 and CREBH pathways. Blood 36 22262759
2016 Hyperlipidemia and hepatitis in liver-specific CREB3L3 knockout mice generated using a one-step CRISPR/Cas9 system. Scientific reports 35 27291420
2010 N-linked glycosylation is required for optimal proteolytic activation of membrane-bound transcription factor CREB-H. Journal of cell science 35 20356926
2012 The role of CREB-H transcription factor in triglyceride metabolism. Current opinion in lipidology 34 22262056
2020 N-glycosylation of CREBH improves lipid metabolism and attenuates lipotoxicity in NAFLD by modulating PPARα and SCD-1. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 33 32996649
2013 Hepatic cannabinoid receptor type 1 mediates alcohol-induced regulation of bile acid enzyme genes expression via CREBH. PloS one 33 23894352
2018 Endoplasmic Reticulum-Bound Transcription Factor CREBH Stimulates RANKL-Induced Osteoclastogenesis. Journal of immunology (Baltimore, Md. : 1950) 32 29378912
2012 Activation of cannabinoid receptor type 1 (Cb1r) disrupts hepatic insulin receptor signaling via cyclic AMP-response element-binding protein H (Crebh)-mediated induction of Lipin1 gene. The Journal of biological chemistry 32 22989885
2007 Trafficking of the bZIP transmembrane transcription factor CREB-H into alternate pathways of ERAD and stress-regulated intramembrane proteolysis. Traffic (Copenhagen, Denmark) 32 17875199
2017 Critical role of CREBH-mediated induction of transforming growth factor β2 by hepatitis C virus infection in fibrogenic responses in hepatic stellate cells. Hepatology (Baltimore, Md.) 30 28621467
2010 Fatty acids regulate CREBh via transcriptional mechanisms that are dependent on proteasome activity and insulin. Molecular and cellular biochemistry 30 20607591
2021 The transcription factors CREBH, PPARa, and FOXO1 as critical hepatic mediators of diet-induced metabolic dysregulation. The Journal of nutritional biochemistry 29 33789150
2020 Loss-of-Function CREB3L3 Variants in Patients With Severe Hypertriglyceridemia. Arteriosclerosis, thrombosis, and vascular biology 28 32580631
2020 CREBH: A Complex Array of Regulatory Mechanisms in Nutritional Signaling, Metabolic Inflammation, and Metabolic Disease. Molecular nutrition & food research 28 32997872
2017 A novel EWS-CREB3L3 gene fusion in a mesenteric sclerosing epithelioid fibrosarcoma. Genes, chromosomes & cancer 26 28569045
2011 Tunicamycin negatively regulates BMP2-induced osteoblast differentiation through CREBH expression in MC3T3E1 cells. BMB reports 26 22118540
2021 Regulation of hepatic circadian metabolism by the E3 ubiquitin ligase HRD1-controlled CREBH/PPARα transcriptional program. Molecular metabolism 25 33592335
2019 Transcriptional profiling of PPARα-/- and CREB3L3-/- livers reveals disparate regulation of hepatoproliferative and metabolic functions of PPARα. BMC genomics 24 30866796
2015 Cyclic AMP Response Element-binding Protein H (CREBH) Mediates the Inhibitory Actions of Tumor Necrosis Factor α in Osteoblast Differentiation by Stimulating Smad1 Degradation. The Journal of biological chemistry 23 25873397
2019 Regulation of hepatic autophagy by stress-sensing transcription factor CREBH. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 22 30912978
2017 CREBH mediates metabolic inflammation to hepatic VLDL overproduction and hyperlipoproteinemia. Journal of molecular medicine (Berlin, Germany) 22 28455595
2016 β-TrCP-mediated ubiquitination and degradation of liver-enriched transcription factor CREB-H. Scientific reports 22 27029215
2016 Loss of Transcription Factor CREBH Accelerates Diet-Induced Atherosclerosis in Ldlr-/- Mice. Arteriosclerosis, thrombosis, and vascular biology 22 27417587
2022 CREBH alleviates mitochondrial oxidative stress through SIRT3 mediating deacetylation of MnSOD and suppression of Nlrp3 inflammasome in NASH. Free radical biology & medicine 21 35926687
2021 CREBH normalizes dyslipidemia and halts atherosclerosis in diabetes by decreasing circulating remnant lipoproteins. The Journal of clinical investigation 21 34491909
2015 Novel CREB3L3 Nonsense Mutation in a Family With Dominant Hypertriglyceridemia. Arteriosclerosis, thrombosis, and vascular biology 20 26427795
2023 A hepatokine derived from the ER protein CREBH promotes triglyceride metabolism by stimulating lipoprotein lipase activity. Science signaling 19 36649378
2020 Enterohepatic Transcription Factor CREB3L3 Protects Atherosclerosis via SREBP Competitive Inhibition. Cellular and molecular gastroenterology and hepatology 19 33246135
2016 Toll-like Receptor (TLR) Signaling Interacts with CREBH to Modulate High-density Lipoprotein (HDL) in Response to Bacterial Endotoxin. The Journal of biological chemistry 19 27637329
2010 Different mechanisms of recognition and ER retention by transmembrane transcription factors CREB-H and ATF6. Traffic (Copenhagen, Denmark) 19 19883396
2015 bZIP transmembrane transcription factor CREBH: Potential role in non-alcoholic fatty liver disease (Review). Molecular medicine reports 18 26718596
2014 Alpha lipoic acid induces hepatic fibroblast growth factor 21 expression via up-regulation of CREBH. Biochemical and biophysical research communications 16 25449271
2015 Activation of hepatic CREBH and Insig signaling in the anti-hypertriglyceridemic mechanism of R-α-lipoic acid. The Journal of nutritional biochemistry 14 26007286
2019 MS-275 induces hepatic FGF21 expression via H3K18ac-mediated CREBH signal. Journal of molecular endocrinology 12 30893641
2022 FACI Is a Novel CREB-H-Induced Protein That Inhibits Intestinal Lipid Absorption and Reverses Diet-Induced Obesity. Cellular and molecular gastroenterology and hepatology 11 35093589
2019 Sclerosing Epithelioid Fibrosarcoma of the Bone With Rare EWSR1-CREB3L3 Translocation Driving Upregulation of the PI3K/mTOR Signaling Pathway. Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society 11 31335288
2023 Hepatic PTP4A1 ameliorates high-fat diet-induced hepatosteatosis and hyperglycemia by the activation of the CREBH/FGF21 axis. Theranostics 10 36793871
2022 The Role and Mechanism of CREBH Regulating SIRT3 in Metabolic Associated Fatty Liver Disease. Life sciences 10 35902030
2021 Inducible hepatic expression of CREBH mitigates diet-induced obesity, insulin resistance, and hepatic steatosis in mice. The Journal of biological chemistry 10 34023388
2020 Synergistic regulation of hepatic Fsp27b expression by HNF4α and CREBH. Biochemical and biophysical research communications 10 32553626
2015 Phosphorylation and SCF-mediated degradation regulate CREB-H transcription of metabolic targets. Molecular biology of the cell 10 26108621
2024 Dietary medium-chain fatty acids reduce hepatic fat accumulation via activation of a CREBH-FGF21 axis. Molecular metabolism 9 39019116
2023 Enhancement of the SESN2-SHP cascade by melatonin ameliorates hepatic gluconeogenesis by inhibiting the CRBN-BTG2-CREBH signaling pathway. Experimental & molecular medicine 9 37488285
2020 CREBH knockout accelerates hepatic fibrosis in mouse models of diet-induced nonalcoholic fatty liver disease. Life sciences 8 32417373
2019 Hepatocyte CREBH deficiency aggravates inflammatory liver injury following chemokine-dependent neutrophil infiltration through upregulation of NF-κB p65 in mice. Archives of toxicology 8 31797000
2021 Starvation-induced transcription factor CREBH negatively governs body growth by controlling GH signaling. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 7 34042217
2024 ER-tethered stress sensor CREBH regulates mitochondrial unfolded protein response to maintain energy homeostasis. Proceedings of the National Academy of Sciences of the United States of America 6 39589874
2021 CREBH Systemically Regulates Lipid Metabolism by Modulating and Integrating Cellular Functions. Nutrients 6 34579081
2024 Molecular characterization of transcription factor CREB3L2 and CREB3L3 and their role in melanogenesis in Pacific oysters (Crassostrea gigas). Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology 5 38604561
2023 CREBH promotes autophagy to ameliorate NASH by regulating Coro1a. Biochimica et biophysica acta. Molecular basis of disease 5 37837948
2018 Co-occurrence of heterozygous CREB3L3 and APOA5 nonsense variants and polygenic risk in a patient with severe hypertriglyceridemia exacerbated by estrogen administration. Journal of clinical lipidology 5 29954705
2017 GSK-3-mediated phosphorylation couples ER-Golgi transport and nuclear stabilization of the CREB-H transcription factor to mediate apolipoprotein secretion. Molecular biology of the cell 5 28381424
2025 Cgref1 is a CREB-H-regulated hepatokine that promotes hepatic de novo lipogenesis by mediating epididymal fat insulin resistance. International journal of biological sciences 4 40303310
2023 CrebH protects against liver injury associated with colonic inflammation via modulation of exosomal miRNA. Cell & bioscience 3 37370191
2021 Adipose expression of CREB3L3 modulates body weight during obesity. Scientific reports 3 34588527
2024 Hypertriglyceridemia-induced acute pancreatitis in pregnancy associated with CREB3L3 mutation. Journal of clinical lipidology 2 39562229
2025 Creb3l3 deficiency promotes intestinal lipid accumulation and alters ApoB-containing lipoprotein kinetics. Journal of lipid research 1 40449732
2026 Sex-specific KDM6A-HNF4A-CREBH network controls lipoprotein cholesterol metabolism and atherosclerosis via epigenetic reprograming of hepatocytes. Nature communications 0 41872164
2025 Rab2A modulates liver fibroblast growth factor 21 (FGF21) expression and systemic metabolism via apolipoprotein B-CREBH signaling. The Journal of biological chemistry 0 41314545
2022 CREBH regulation of lipid metabolism through multifaceted functions that improve arteriosclerosis. Journal of diabetes investigation 0 35122696
2013 CREBH determines the severity of sulpyrine-induced fatal shock. PloS one 0 23409047

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