Dimerization of hub protein DYNLL1 and bZIP transcription factor CREB3L1 enhances transcriptional activation of CREB3L1 target genes like arginine vasopressin.
Reduced CREB3L1 expression in triple negative and luminal a breast cancer cells contributes to enhanced cell migration anchorage-independent growth and metastasis.
Study reports a novel homozygous CREB3L1 mutation in a large Indonesian family with osteogenesis imperfecta (OI); the homozygous affected members have survived to adulthood and they present a more severe phenotype than previously reported expanding the clinical spectrum of OI for this gene.
Here we presenta Turkish family in which molecular analysis of the proband revealeda previously unreported homozygous missense variant(c.911C>T p.(Ala304Val))of the CREB3L1
These results suggest that CREB3L1 expression level may be used as a biomarker to identify TNBC patients who are more likely to benefit from doxorubicin-based chemotherapy.
There was a relationship between the expression levels of both proteins and survival time. CREB3L1 and PTN expression levels serve as biomarkers with utility in grading gliomas. Absence of CREB3L1 and presence of PTN in brain glioma cells correlate with survival time of the glioma patients.
Our findings support a model in which CREB3L1 acts as a downstream effector of TSH to regulate the expression of cargo proteins and simultaneously increases the synthesis of transport factors and the expansion of the Golgi to synchronize the rise in cargo load with the amplified capacity of the secretory pathway
ConclusionThis report confirms that CREB3L1 is an OI-related gene and suggests the pathogenic mechanism of CREB3L1-associated OI involves the altered regulation of proteins involved in cellular secretion.
Identification of novel prostate cancer drivers ERF CREB3L1 and POU2F2 using RegNetDriver a framework for integration of genetic and epigenetic alterations with tissue-specific regulatory network.
These findings indicate that the miR-146a-CREB3L1-FGFBP1 signaling axis plays an important role in the regulation of angiogenesis in human umbilical vein endothelial cells.
The results suggest that CREB3L1 is required for decidualization in mice and humans and may be linked to the pathogenesis of endometriosis in a progesterone-dependent manner.
Our data further strengthens the role for CREB3L1 as a metastasis suppressor in breast cancer and demonstrates that epigenetic silencing is a major regulator of the loss of CREB3L1 expression
CREB3L1 was expressed in 19% of RCC which is generally resistant to doxorubicin but in 70% of diffuse large B-cell lymphoma that is sensitive to doxorubicin.
CREB3L1 mRNA expression is downregulated in human bladder cancer.CREB3L1 is epigenetically silenced in human bladder cancer facilitating tumor cell spreading and migration in vitro.
Cleavage of CREB3L1 releases its NH2-terminal domain from membranes allowing it to enter the nucleus where it binds to Smad4 to activate transcription of genes encoding proteins required for assembly of collagen-containing extracellular matrix.
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