This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
4 Q&As
Facts about Transcriptional repressor protein YY1.
The impact on transcription regulation is depending on the context in which it binds and diverse mechanisms of action include direct activation or repression, indirect activation or repression via cofactor recruitment, or activation or repression by disruption of binding sites or conformational DNA changes. Its activity is regulated by transcription factors and cytoplasmic proteins that have been shown to abrogate or completely inhibit YY1-mediated activation or repression.
Human | |
---|---|
Gene Name: | YY1 |
Uniprot: | P25490 |
Entrez: | 7528 |
Belongs to: |
---|
YY transcription factor family |
Delta transcription factor; DELTA; INO80SYY-1; NF-E1; NF-E1INO80 complex subunit S; transcriptional repressor protein YY1; UCRBP; Yin and Yang 1 protein; Yin and yang 1; YIN-YANG-1; YY1 transcription factor; YY1
Mass (kDA):
44.713 kDA
Human | |
---|---|
Location: | 14q32.2 |
Sequence: | 14; NC_000014.9 (100239144..100282788) |
Nucleus matrix. Associated with the nuclear matrix.
If you're seeking information on the YY1 marker If so, you're at the right site. It's an inhibitor of transcriptional repressors that block tumor cell proliferation, regulates cell migration, and regulates the expression of immune cells. The informationgraphics for genes on the Boster site contain basic details about each gene, including the function and significance. You can also use the search bar to locate the gene you're interested in.
The transcriptional factor YY1 that regulates a wide range of gene expression, including the ones that encode genes important for regulating the immune system. Overexpression of YY1 can result in decreased muscle strength and fewer fibers for COPD patients. In addition, YY1 is also associated with decreased strength and COPD-related quadriceps atrophy.
The YY1 gene is an essential element of the nucleus of a cell, since it plays a significant role in the process of organogenesis and progression of cancer. In this study, YY1 was expressed in HeLa cells that stably expressed wild type, Y383E or Y383F YY1 mutants. The cells were then analyzed for RNA by RTPCR , to determine if YY1-responsive mRNA was c–fos.
YY1 is a partner to HDAC5 (a protein that plays a role in the expression and repression of gene expression) and PP2A (a protein involved in that process). The interaction between YY1 and HDAC5 takes place only in differentiated cells. Because YY1 is necessary to differentiate muscles interactions with HDAC5 are crucial to its function. Additionally, interactions with HDAC5 might be crucial to maintaining the final differentiation of muscle cells.
Although YY1 is found in adult muscle groups, it is not a prominently expressed protein in the muscle. Therefore, we needed to isolate the protein by means of immunoprecipitation and then immunoblotting to analyze its levels. To analyze YY1, it required between three and six micrograms of protein.
The YY1 gene is a novel tumor suppressor that negatively regulates cell proliferation and tumor growth through inhibition of several pathways. YY1 blocks c-Myc and inhibits miR-141/PTEN expression. This inhibitory effect was evident in both metastatic and primary cancer cells. Restoring miR-141 expression partially reversed the inhibition of cancer growth.
Although the YY1 marker has a dual biological role in various cancer types the role it plays in nasopharyngeal tumors isn't yet established. The HNE2 and 5-8F cell line overexpress the YY1 marker and inhibit cell proliferation in colony development tests. This study suggests that YY1 could play a role in the treatment of this type of cancer.
By using a lentiviral expression molecule that contains the complete ORF of human YY1, the firm created a lentiviral treatment to restore miR-141 and boosts YY1 protein levels. The viral and lentiviral particles were co-transfected into HEK293T cells. After 38 days, the cells were destroyed. The tumor grafts were then inserted.
The boster bio YY1 marker also blocks xenografted renal cancer cells by inhibiting their proliferation. Nobiletin blocks the pathway between the SRC and the AKT and the expression of YY1AP1 in cancer cells. These two tumor suppressors could be used to help in the treatment of a variety of cancer-related diseases.
Boster Bio's YY1 marker regulates CASC11 expression which is a marker that blocks cell movement. CASC11 has been shown to play a role in DNA replication and is considered a marker of cell proliferation. This protein has been shown to block cell invasion and migration. Here, we describe how this protein hinders the migration of Caki-2 and ACHN cells.
TPD52 plays a role not only in breast cancer cell proliferation and migration but also influences the expression of proteins of importance. To assess the role of TPD52 in cell proliferation and migration BT474 cells were transfected with siTPD52-1 or -2. Cell proliferation and migration was examined using the Transwell assay and western blotting and western blotting, respectively. Results revealed that Boster bio YY1 slowed both migration and cell proliferation.
To determine if they control cell proliferation and/or migration The YY1AP1 and STAT3 proteins were examined. Caki-2 cells showed an increase in STAT3 activity and ACHN cell proliferation after STAT3 inhibition. However, treatment with nobiletin inhibited the nuclear translocation of STAT3 and YY1AP1 in Caki-2 cells.
YY1 is a tumor suppressor gene that has been associated with the development of TAM. Its promoter sequences are linked to the miR-125a promoter in order to inhibit the expression of this RNA. Furthermore, YY1 has been demonstrated to regulate the expression of miR-125a, which is a key regulator of immune cell function. Because of its role in the immune system, YY1 might aid in the development and maintenance of TAMs.
The YY1 protein plays a key role in the development of LTHSCs, which are the progenitors of skeletal muscles and heart. Its overexpression in these cells is linked to the increased expression of lymphoid-derived cell. It has been demonstrated that YY1 expression is not positively associated with the development of B cells. In addition, the overexpression of YY1 has been linked with antitumor treatments resistance.
YY1 can also play a role in regulating tumor-related tissues, where it can cause alterations in cell growth and viability. It has a number of common properties with cancer stem cells, including regulatory roles in the epithelial-mesenchymal transition and metastasis. YY1 overexpression can also affect the expression of other proteins within the tumor-bearing microenvironment, such as SOX2, NANOG and BMI1.
The YY1 gene plays an important part in the growth of the embryo. A mouse model of YY1 is required to determine whether it plays a role in embryonic stemness. Donohoe and his coworkers proved that YY1 knockout mice could be fatal at an early stage. They were characterized by a blastocoelic cavity, and ICM. In addition, they demonstrated that YY1 downregulation lowered the expression of master regulators of embryogenesis, like Sox2 and Oct4, and also increased the expression of trophoblasts.
The discovery of PTPN12 might be a helpful diagnostic biomarker for Esophageal cancer. This gene has been associated with a variety of digestive tract cancers, including ESCA and STAD. Although PTPN12 is in the beginning stages of development, it has been linked to a variety of gastrointestinal cancers. It might also be useful as a biomarker in CRC.
Researchers used the Ualcan database to determine the expression of PTPNs in ESCA and normal tissue. The same protein was discovered to be elevated in STAD COAD, STAD, and READ tumors and decreased in ESCA tissues. Furthermore, PTPN22 was also discovered to be deficient in the tissues of patients. This finding is still being confirmed by ESCA.
Researchers are studying whether YY1 could be a viable option for a novel therapy. The YY1 marker blocks the formation of p21WAF1 and binds with the c-myc promotor. If this is true, it might be a possible therapeutic target for HCC. The YY1 gene is widely circulating and conserved. Its role in the fight against cancer is not clear, but the gene is known to interact with HDACs.
The YY1 marker blocks the growth of tumors with downregulation of miR-141. The company has conducted coIP experiments with total protein extracts, which have shown that the overexpression of YY1 decreases the expression levels of c-Myc as well as the Max/Mad complex by 71%. This suggests that YY1 blocks cMyc's transcriptional activity towards the target gene. It also blocks cMyc binding to Ebox sequences which is crucial to the development of targeted cancer treatments.
This study also demonstrates that tumors that express YY1 had shorter overall survival times than tumors that had low expression of BMAL1. Kaplan-Meier analyses revealed that patients with high miR-135b and low BMAL1 expression had significantly lower overall survival rates than patients without miR-141 expression. Multivariate Cox regression analysis was used to adjust for AJCC stage, T/N class cancer location gender, age and other factors.
PMID: 1655281 by Shi Y., et al. Transcriptional repression by YY1, a human GLI-Kruppel-related protein, and relief of repression by adenovirus E1A protein.
PMID: 1946405 by Park K., et al. Isolation of a candidate repressor/activator, NF-E1 (YY-1, delta), that binds to the immunoglobulin kappa 3' enhancer and the immunoglobulin heavy-chain mu E1 site.