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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.
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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.
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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.
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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
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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.
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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.
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Ceramide inverts the membrane orientation of TMS4SF20, creating a form of TM4SF20 that stimulates the cleavage of CREB3L1.
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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.
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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
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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.
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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.
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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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CREB3L1 expression may be a useful biomarker in identifying cancer cells sensitive to doxorubicin.
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Case Reports: genetically confirmed primary renal sclerosing epithelioid fibrosarcoma with EWSR1-CREB3L1 gene fusion.
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Case Report: low-grade fibromyxoid sarcoma of the kidney found to harbor the EWSR1-CREB3L1 gene fusion.
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Temporally regulates the differentiation from neural precursor cells into astrocytes [review]
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EWSR1-CREB3L1 gene fusions are predominant over FUS and CREB3L2 rearrangements in pure sclerosing epithelioid fibrosarcoma.
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CREB3L1 plays an important role in suppressing tumorigenesis and that loss of expression is required for the development of a metastatic phenotype.
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Fbxw7 controls osteogenesis and chondrogenesis by targeting OASIS and BBF2H7, respectively, for degradation.
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a novel regulatory mechanism for VEGFA transcription by OASIS in human retinal pigment epithelial cells
