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- Table of Contents
Facts about Transcription factor 7-like 1.
Participates in the Wnt signaling pathway.
Binds to DNA and acts as a repressor in the absence of CTNNB1, and as an activator in its presence.Necessary for the terminal differentiation of epidermal cells, the formation of keratohyalin granules and the development of the barrier function of the skin. .
Mouse | |
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Gene Name: | Tcf7l1 |
Uniprot: | Q9Z1J1 |
Entrez: | 21415 |
Belongs to: |
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TCF/LEF family |
HMG box transcription factor 3; TCF3; TCF-3; TCF7L1; transcription factor 7-like 1 (T-cell specific, HMG-box); transcription factor 7-like 1
Mass (kDA):
62.298 kDA
Mouse | |
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Location: | 6 C1|6 32.27 cM |
Sequence: | 6; |
Detected in the basal layer of epidermis and in outer root sheath and bulge of hair follicles.
This article will discuss the clinical applications and functions of the TCF7L1 marker. It will provide you with useful information about this marker, including its specificity and sensitivity. Boster scientists have the ability to submit their results to specific species, applications, samples, and other subjects. These results can be used by scientists from all over the world. You can learn more about Boster Bio by reading on!
There are many uses for the TCF7L1 (transcription factor 7-like 1 marker). This protein is part a larger network of transcription factors that regulate pluripotency. It negatively regulates Nanog's transcription and mediates the shift from naive to primed pluripotent states. The TCF7L1 gene also serves many other functions in the human body.
TCF7L1 acts as a transcriptional regulator in the absence of Wnt signaling. This has been demonstrated by biochemical activity and loss-of-function phenotypes. TCF7L1 directly suppresses the sox4a genes. Although its function is not fully understood, it appears to be important for maintaining the progenitor status.
TCF7L1 may be used as a marker for a specific gene or condition. A genetic test might help you find the best way of treating a condition. TCF7L1 can be used for genetic counseling. For example, if you suffer from high blood pressure, you should consider taking a course on how to reduce the risk of stroke. If you have a family history with TCF7L1 deficiency in your family, you might consider using this gene for your research.
TCF7L1 can be expressed in adipocytes. It represses genes which are essential for the formation and maintenance of mature adipocytes. Its binding sites are enriched for pathways involved in cell structure. TCF7L1 also colocalizes well with HDAC1. Additionally, H3K9Ac levels are reduced in cells that express TCF7L1.
TCF7L1 is a gene involved in cardiac linage development. However, its function is not clear. Despite the ligand-dependent nature of its transcriptional activities, Tcf7l1 appears to function independently of b-catenin. It could also interact with LCN2, which is required for its transactivation. In addition, it is unknown whether Tcf7l1 functions in the cardiac artery.
TCF7L1 overexpression promoted skin cancer growth in a mouse model. TCF7L1 was also found to increase the weight of xenografted skin cancers. These tumors were derived from skin SCC cell lines, SCC13 and SRB12.
It is not known how TCF7L1-overexpression contributes to tumor development. However, it is known that overexpression of TCF7L1 may help tumor cells survive senescence. Overexpression of this gene can promote tumor growth by inhibiting HRAS-induced, senescent senescence. It is not known what mechanisms underlie TCF7L1’s tumor-promoting properties. It has been demonstrated that TCF7L1 mRNA levels are associated with shorter survival rates in colorectal carcinoma. TCF7L1 was also found to decrease the growth of colorectal tumor cells and the size of xenografted sarcomas.
TCF7L1 belongs to a complex network that regulates the pluripotency state. It negatively regulates Nanog transcription and mediates transition from a naive pluripotent state to a primed one. It is essential for differentiation of ESCs into different tissue types. The ESCs will not be able to differentiate properly if the TCF7L1 gene mutation causes a poor outcome.
TCF7L1 plays a critical role in cardiac differentiation. Tcf7l1 inhibits cardiac differentiation in zebrafish. However, its loss of function promotes endothelial speciation. In other species, TCF7l1 may play different roles. Other TCF/LEF genes may have compensated for the loss of this gene. Moreira et al. Moreira et.al. showed that one TCF/LEF-related factor can induce trilineage in ESCs. These findings suggest that TCF/LEF factor interactions facilitate organogenesis.
TCF7L1 can be found in the hypothalamus as well as the developing pituitary. The gene regulates WNT/b–catenin pathway and is expressed in developing forebrain. This gene is implicated in the formation of the HP axis. However, its role is not well understood in cancer.
Dysregulation of the Wnt pathway is a hallmark of colorectal cancer. Among its target genes, CTNNB1 acts as a transcriptional coactivator that promotes the expression of a broad set of genes, including those that promote tumor growth. CTNNB1's interactions with transcription factors are unknown. Some of these targets may be oncogenic, while others regulate differentiation. The TCF7L1 gene is thought to buffer CTNNB1-induced target genes expression. Loss of TCF7L1 significantly impaired the growth of HCT116 cells and reduced tumor growth in a mouse xenograft model.
The TCF7L1 marker is highly specific for a subset of neurons. This gene can be found in the neocortex VZ, ganglionic eminences and GE. TCF7L1 plays a key role in neuronal growth and cell-cell interactions. It is also negatively associated to androgen receptor signaling.
Three types of cell lines were used to test the expression levels of TCF7L1. AR-negative cells expressing TCF7L1 overexpressed in PC3 cells were found to have increased cell invasion and migration abilities but not proliferation. TCF7L1 was not expressed in cells. WNT4 treatment was ineffective on these cells. Thus, TCF7L1 overexpression in a mouse model was a sensitive marker of pancreatic cancer.
Kuwahara and colleagues found that shRNA inhibited Tcf7L1 in vitro, leading to increased neuronal differentiation. However, Tcf7L1 electroporation in utero resulted is decreased neuronal division. However, these results were not reliant on a genetic approach to confirm the role of TCF7L1 in cortical neurogenesis.
TCF7L1 in tumors of high or low grade was identified in the present study. TCF7L1 in PCa was also found to be associated CXCR2, IL-8, as well as WNT4. These findings suggest that TCF7L1 promotes NED. These findings support the hypothesis of TCF7L1 being a novel marker that can help identify prostate cancer patients with an androgen-receptive genotype.
The TCF7L1 gene is regulated by IL-8/CXCR2 signaling pathways. This crosstalk between cytokine signaling and WNT signaling is linked to the progression of NEDPCa. It is therefore an important marker for NED. It is also likely to improve patient care. The TCF7L1 gene is a crucial regulator of a cell's function.
Availability of the TCF7L1 gene marker in Boster bio can be used to identify pluripotency-associated genes, such as PD and CSC, in various human cell types. This marker can also be used to detect PD-related cancers. The marker provides information on the cellular processes involved in PD. The following genes are included on the list:
The NAV2 genome is located on chromosome 11. It's joined with the 3’ coding segment of TCF7L1 onto chromosome 2. TCF7L1 is part of the TCF/LEF transcribing factors family. It heterodimerizes to nuclear b–catenin. The NAV2-TCF7L1 mutation protein is missing TCF3’s binding domain. Multiple cancer samples have shown that TCF7L1 gene markers are available in Boster Bio.
PMID: 9488439 by Korinek V., et al. Two members of the Tcf family implicated in Wnt/b-catenin signaling during embryogenesis in the mouse.
PMID: 10498690 by DasGupta R., et al. Multiple roles for activated LEF/TCF transcription complexes during hair follicle development and differentiation.