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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.
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.
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
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.
Ceramide inverts the membrane orientation of TMS4SF20, creating a form of TM4SF20 that stimulates the cleavage of CREB3L1.
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.
CREB3L1 expression may be a useful biomarker in identifying cancer cells sensitive to doxorubicin.
Case Reports: genetically confirmed primary renal sclerosing epithelioid fibrosarcoma with EWSR1-CREB3L1 gene fusion.
Case Report: low-grade fibromyxoid sarcoma of the kidney found to harbor the EWSR1-CREB3L1 gene fusion.
Temporally regulates the differentiation from neural precursor cells into astrocytes [review]
EWSR1-CREB3L1 gene fusions are predominant over FUS and CREB3L2 rearrangements in pure sclerosing epithelioid fibrosarcoma.
CREB3L1 plays an important role in suppressing tumorigenesis and that loss of expression is required for the development of a metastatic phenotype.
Fbxw7 controls osteogenesis and chondrogenesis by targeting OASIS and BBF2H7, respectively, for degradation.
a novel regulatory mechanism for VEGFA transcription by OASIS in human retinal pigment epithelial cells
OASIS is important for the ER stress response and maintenance of some extracellular matrix proteins in human glioma cells.
The endoplasmic reticulum stress transducer old astrocyte specifically induced substance (OASIS) positively regulates glial scar formation in spinal cord injury (SCI). OASIS deletion inhibited the development of N-cadherin-positive reactive astrocytes that form glial scars and promoted axon growth and functional recovery after SCI.
OASIS affects the expression of HIF-1alpha target genes through the protein interaction with HIF-1alpha, and that OASIS-HIF-1alpha complexes may play essential roles in angiogenesis during bone development.
Higher levels of CREB3L1 protein are correlated with increased doxorubicin sensitivity of xenograft RCC tumors
Increased susceptibility to dextran sulfate sodium-induced colitis in the endoplasmic reticulum stress transducer OASIS deficient mice.
We conclude that OASIS functions as an anti-regenerative transcription factor by establishing a non-permissive microenvironment to regenerating axons
Gliosis-specific transcription factor OASIS coincides with proteoglycan core protein genes in the glial scar and inhibits neurite outgrowth.
Findings demonstrate a novel mechanism by which OASIS and its associated family members are modulated by the unfolded protein response to finely control astrocyte differentiation.
OASIS plays crucial roles in promoting the differentiation of early goblet cells to mature goblet cells in the large intestine.
OASIS may play a role in bone formation through the expression of type I collagen and the secretion of bone matrix proteins in fracture healing.
OASIS regulates skeletal development by osteoblast-dependent and -independent mechanisms.
OASIS-/- mice exhibit severe osteopenia involving a decrease in type I collagen in the bone matrix and a dysfunction of osteoblasts, which show abnormal expansion of the rough ER.
Data suggest that OASIS protein positively regulates gene transcription in a subset of reactive astrocytes, and may influence the reaction of injured central nervous system tissues [OASIS protein].
In mice, the OASIS gene may be related to proteoglycan expression and play a role in the differentiation of the odontoblast and cells in inner enamel epithelium.
Our results reveal pivotal roles for OASIS in modulating the unfolded protein response in astrocytes, and the possibility that cell type-specific UPR signalling also exists in other cells
Oasis is an endoplasmic reticulum stress transducer in astrocytes, a membrane-bound transcription factor that activates genes in the stress response.
OASIS expressed in astrocytes plays important roles in protection against kainic acid-induced damage to hippocampal pyramidal neurons.
Signalling mediated by the endoplasmic reticulum stress inducer Oasis is involved in bone formation.
Transcription factor that acts during endoplasmic reticulum stress by activating unfolded protein response target genes. Specifically involved in ER-stress response in astrocytes in the central nervous system. May play a role in gliosis. In vitro, binds to box-B element, cAMP response element (CRE) and CRE-like sequences, and activates transcription through box-B element but not through CRE (By similarity).
cAMP responsive element binding protein 3-like 1
, cyclic AMP-responsive element-binding protein 3-like protein 1-like
, BBF-2 homolog
, cAMP-responsive element-binding protein 3-like protein 1
, cyclic AMP-responsive element-binding protein 3-like protein 1
, old astrocyte specifically-induced substance
, old astrocyte specifically induced substance