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- Table of Contents
Facts about Cyclic AMP-responsive element-binding protein 3-like protein 1.
In response to ER stress, transported to the Golgi, where it is cleaved at a site-specific manner by resident proteases S1P/MBTPS1 and S2P/MBTPS2. The published N-terminal cytosolic domain is translocated into the nucleus to influence transcription of specific target genes.
Mouse | |
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Gene Name: | Creb3l1 |
Uniprot: | Q9Z125 |
Entrez: | 26427 |
Belongs to: |
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bZIP family |
BBF-2 Homolog; cAMP responsive element binding protein 3-like 1; cAMP-responsive element-binding protein 3-like protein 1; CREB3L1; OASIS; OASIScyclic AMP-responsive element-binding protein 3-like protein 1; old astrocyte specifically induced substance; Old astrocyte specifically-induced substance
Mass (kDA):
56.959 kDA
Mouse | |
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Location: | 2|2 E1 |
Sequence: | 2; |
Expressed in cortical and trabecular bones. Highly expressed in osteoblasts, but not detected in osteoclasts, nor in macrophages (PubMed:19767743). Expressed at relatively low levels in lung and kidney. Weakly expressed in brain and spleen.
CREB3L1 has been linked to the p53 signaling pathways and mTORC1 pathway, but it is also used for a variety biological assays. This guide will explain how to optimize your experiments as well as the different applications of this marker. It is also possible to use Boster Bio troubleshooting guides to discover the root of your error. Boster Bio troubleshooting tools can assist you in fixing the problem no matter what your research goals.
Recent research has shown that CREB3L1 in various types of cancers is a bad prognosis indicator. The significance of this marker can be determined by its high SS or low SS. The SS is a statistical indicator of CREB3L1 nucleus localization. However, further research is necessary to determine the prognostic impact of CREB3L1.
One of the primary reasons for CREB3L1 to be a poor prognosis marker is its role in the suppression of metastasis. The protein is present in cells with limited metastatic potential. The loss of this protein could signal poor prognosis. However, there is no any consensus regarding the exact role of CREB3L1 for the suppression of metastasis.
Researchers found that doxorubicin sensitivity was higher in patients with RCC tumors that are xenografts. Because of its high sensitiveness, doxorubicin was not shown to be a reliable treatment for RCC. CREB3L1 is also found in 70% of patients suffering from diffuse large-cell lymphoma.
Many studies have found that a lack of CREB3L1 is associated with a poor prognosis when it comes to cancer. While the mechanism behind this phenomenon is not known hypoxia-induced stress and the tumor microenvironment have been found to activate the UPR. The gene is involved in the growth and metastasis of breast cancer. Breast cancer metastatic cells that lack the CREB3L1 gene had less growth, invasion, survival and hypoxic conditions.
Researchers have also discovered that patients with high CREB3L1 expression had smaller blood vessels. Additionally, the number of large blood vessels was reduced. However this result was not statistically significant when compared with patients with low expression of CREB3L1.
The signaling pathway p53 plays numerous roles to play in the survival of cancer cells. One of these roles is in the regulation of angiogenesis. This pathway is involved in angiogenesis induced by tumors. Increased expression of FGFbp1 and pleiotrophin stimulate the development of tumors. CREB3L1 interacts with the promoters of these genes and inhibits them expression.
The CREB3L1 gene is associated with many cellular processes. CREB3L1 is involved in the regulation of EMT and the mTOR pathway. It is also a component of the highly conserved transcription factor NFYA. Furthermore, CREB3L1 is involved in ATC development. It also participates in the signaling pathway of p53, and mTOR.
Dedifferentiation is an important feature of thyroid cancer and is a poor prognosis. Researchers have been able trace the path of thyroid cancer by using single-cell RNA sequencing. The development course revealed that anaplastic cells originate from papillary thyroid cancer cells. The functional role of CREB3L was further revealed by the transcriptional regulatory network.
Other signaling pathways in addition to p53 are involved. Module 1 involved 59 crucial nodes. They include the p53 signaling pathway, cell cycle, and progesterone-mediated oocyte maturation. Module 2 dealt with protein digestion and absorption. Module 3 dealt with the IL-17 pathway, complement and coagulation. Interestingly, CREB3L1 & NFYB are both associated with p53 signaling pathways.
Cell death is correlated with activation of the p53 pathway. It is believed that CREB3L1 may be involved with the p53 signaling pathway that regulates the expressions of various CDKs/cyclins. ATR and ATM are phosphorylates of the E3 Ubiquitin Ligase SIAh2 and prevent mitosis.
The molecule CREB3L1 is that is associated with the mTORC1 signaling pathway. It is also connected to other signaling pathways, such as the MAPK cascade. Cellular transformation is affected by the downstream effectors of mTOR signaling. These genes are associated with poor outcomes in cancer, and with conditions like Peutz-Jeghers and Cowden's Syndrome. It is linked to the energy-stress response, cell differentiation and drugs administration genes.
Research on cancer has linked the mTOR pathway to the development of tumors, metastasis, and invasion. Activation of this pathway is linked to a range of illnesses, including cancer, arthritis, and insulin resistance. In the field of cancer research, it has become a popular target for therapeutic intervention. Recent research has demonstrated that mTOR inhibitors may reduce the growth of cancer cells.
The CREB3L1 transcription factor is part of a group of transcription factors. It is linked to mTORC1 signaling pathway and helps to promote cell growth and development. It regulates a variety of processes related to the mTOR pathway including cell differentiation, protein production, and immune responses. Although mTOR may not be the only factor associated with CREB3L1, it plays an important role in the mTORC1 pathway.
The mutation of liver kinase A1 causes activation of mTORC1. AKT phosphorylates PRAS40, which negatively regulates mTORC1.
CREB3L1 is part of the CREB family. It plays a role in the secretion process, hormone production, extracellular matrix formation, cellular proliferation, and ER stress. It also activates mmp9 promoter activity. Many biological tests utilize this protein. This article will review its role in vascular diseases, and the possible mechanism of action.
CREB3L1 is a transcription factor that is directly linked to the G-box motif on the promoter of the gene. It has been implicated with many diseases, including Parkinson's disease and Alzheimer's. Studies of the molecular structure of Creb3l1 have identified a direct link between the protein and a range of neurodegenerative diseases.
In recent years, researchers have studied Creb3L1 expression in human hepatoma cell lines. They discovered that activation of CREB3L1 blocks hepatitis C virus replication. The activation of CREB3L1 is controlled by intramembrane proteolysis, while nuclear CREB3L1 interacts with promoters and inhibits the growth of infected cells.
In tumors, CREB3L1 expression is strongly related to the development of metastases and cancer cells. In addition, metastatic breast cancer cells that have this protein are less likely to develop tumors or spread throughout the body. They also do not create metastases. These results suggest that CREB3L1 may be an important tumor suppressor. Researcher? Check out CREB3L1 or other related gene expressions.
As previously mentioned, exome sequencing of CREB3L1 gene was performed by the University of Washington Center for Mendelian Genomics. Sanger sequencing confirmed the variations. InVivo Biosystems offers customized genome edited clones as well as Cas9-Expressing Lines to acquire the mRNA of the CREB3L1 gene. Luciferase-expressing cells are also available for CREB3L1 expression.
Breast cancer patients with triple-negative tumors could be molecularly profiled using CREB3L1 gene. It was discovered in the lab that CREB3L1 overexpression may increase the ability of cells to migrate and reduce E-cadherin expression. However, PTC cells that lacked the expression of CREB3L1 were difficult distinguish from ATC. A positive IHC staining could guide clinical care.
PMID: 10350641 by Honma Y., et al. Identification of a novel gene, OASIS, which encodes for a putative CREB/ATF family transcription factor in the long-term cultured astrocytes and gliotic tissue.
PMID: 12480185 by Nikaido T., et al. Expression of OASIS, a CREB/ATF family transcription factor, in CNS lesion and its transcriptional activity.