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- Table of Contents
Facts about DNA-binding protein SATB1.
Transcriptional repressor controlling nuclear and viral gene expression in a phosphorylated and acetylated status-dependent manner, by binding to matrix attachment regions (MARs) of DNA and inducing a local chromatin-loop remodeling. Acts as a docking site for many chromatin remodeling enzymes (e.
Human | |
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Gene Name: | SATB1 |
Uniprot: | Q01826 |
Entrez: | 6304 |
Belongs to: |
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CUT homeobox family |
DNA-binding protein SATB1; SATB homeobox 1; SATB1; special AT-rich sequence binding protein 1 (binds to nuclearmatrix/scaffold-associating DNA's); Special AT-rich sequence-binding protein 1
Mass (kDA):
85.957 kDA
Human | |
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Location: | 3p24.3 |
Sequence: | 3; NC_000003.12 (18345377..18445592, complement) |
Expressed predominantly in thymus.
Nucleus matrix. Nucleus, PML body. Organized into a cage-like network anchoring loops of heterochromatin and tethering specialized DNA sequences. When sumoylated, localized in promyelocytic leukemia nuclear bodies (PML NBs).
If you're in search of an antibody that isn't available you should think about submitting your specimen to Boster Bio. Boster Bio validates its antibodies on multiple platforms with known positive and negative samples to ensure high affinity and specificity. Boster also rewards the first reviewer of their products with product credits and acknowledges the work of scientists from all over the world. How do you get the most out of your new antibody? Here are some tips:
The profile of expression for SATB1 in breast cancer cells suggests that this protein could influence DNA repair. SATB1 was identified as a target gene for PARP1, TREX2, and RFC4 using transcription profiling assays.
Although we don't know anything about the role of SATB1 and its impact on the development and progression of cancer, it's associated to poor prognosis for many types of cancer. SATB1 is also believed to regulate the development and behavior of several types of cancer. The protein is found in many organs, including the gastrointestinal tract, colon and liver. However, more research is needed to understand more about SATB1's roles in cancer.
SATB1 is a transcriptional element that binds specific sequences of base-unpairing at specific locations. These sequences are then anchored into the nuclear network. These DNA sequences form loops that are connected to chromatin structure. This is a way to ensure the growth and survival of cancer cells. SATB1 plays a role in the development and maintenance of neural cells. It is found in many tissues, including the brain. It is therefore a key transcription factor for the human breast cancer.
Boster Bio, a new genomics firm, has made an important discovery in cancer research: the SATB1 marker controls the epithelial-mesenchymal transition. This process is crucial for cancer progression, metastasis, and chemoradioresistance. The epithelial cells shed their mesenchymal-specific markers and undergo a transition. A majority of human cancers suffer from dysregulation of SATB1, which is responsible for the reversion of EMT and regulates matrix metaloproteinases.
The nuclear protein SATB1 regulates numerous biological processes. Knockdown of SATB1 decreases cell proliferation, invasion, and chemoradiation resistance of NPC cells. MMP-9 and E-cadherin also get reduced by knockdown of SATB1. SATB1 knockdown may also decrease the cell's resistance to radiation and other drugs.
This study proved that SATB1 knockdown reduced cell proliferation and increased apoptosis. These results are not in line with previous studies. The SATB1 marker produced by the company is utilized in cancer cell lines such as T24 and BIU87. It is unclear how this effect might be connected to apoptosis however, these findings support the notion that SATB1 acts as an important regulator of cell death.
A transcription factor critical for embryonic development TWIST is abnormally activated in many cancers. This gene is crucial in epithelial-to-mesenchymal transition (EMT), which is a key step in the progression of cancer. The invasion of tumors and metastasis are the two most significant causes of mortality in Esophageal cancer. In this study, we tried to identify the mechanism by which TWIST regulates the process involved in esophageal tumors.
DNA-binding proteins are often utilized in biological tests. Boster Bio develops SATB1 antibodies that attach to the protein. The protein is present in a wide variety of animal specimens and is believed to be able to understand the sugar-phosphate structure in double-stranded DNA. It regulates the expression of over 1,000 genes. Recent research suggests that it may be an important regulator of the progression of breast cancer.
It is not clear what role SATB1 has in gastric cancer cells. A previous study however has proven that SATB1 can increase the gastric cancer cells. The researchers examined the SATB1 treatment using the SGC7901 cell line. These results are the result of three independent tests. SATB1 has also been shown to block the apoptosis of gastric cancer cells caused by the VCR.
Cells derived from SGC7901 were treated with 1 mg/ml VCR and then plated into 24-well plates. Cells were stained with PI at 50mg/ml after treatment. This allowed for the analysis of the apoptotic indicator. Cells that expressed SATB1 had a lower apoptotic score than cells with SATB1 depleted.
The SATB1 gene encodes a cell component that is involved in the regulation of cell cycle and DNA repair. SATB1 has a dissociation rate that is 0.2 millimeters and is unique to other proteins. Furthermore, it is able to bind to the promoter region of Gp91phox. This indicates that SATB1 can attach to this region.
It is the biological part of the nucleus, made consisting mainly of DNA and RNA. Chromatin is organized into domains through interfacing with the nuclear matrix. These structures are referred to as matrix attachment regions. DNA sequences that preferentially connect to these structures are referred to as attachment regions. These DNA sequences are approximately 200 bp long and contain a topoisomerase 2 consensus sequence. 2. These regions are filled with binding sites.
The nucleus's structure matrix facilitates the formation DNA loop domains that attach with matrix attachment regions. MARs play a crucial role in the regulation of cell cycles and reduce expression variance in transformants. They also function as the origin for DNA replication. Several MARBPs have been identified in plants, animals, and humans. All of them belong to a complex of proteins called co-repressor/co-activator proteins (CR/ACP) and play a role in chromosome folding and gene expression.
The metastasis-associated gene 1 (MTA1) has been implicated in carcinogenesis and metastasis, but it has also been associated with poorer survival in a number of cancer types. Recent studies have shown that MTA1 has been linked to lower survival rates overall in NPC. The protein regulates cytoskeleton of actin restructuring and promotes metastasis in NPC cells.
Knockdown of GLRX3 blocks the growth of the NPC cell line HONE1 in vitro. Eliminating the GLRX3 gene with shGLRX3 construct in HONE1 and CNE2 cells was confirmed using Western Blots. We also measured the number of colonies in cells with and without GLRX3 knockdown using representative colony images. Quantification of the colonies showed a significant difference in GLRX3-knocked-down cells.
In the present study, FGFR4 was identified in a variety of human NPC cell lines that were collected from the Affiliated Hospital of Guangdong Medical University in Zhanjiang, China. The clinical processes were approved by the Institutional Review Board of Guangdong Medical University, and the study was conducted after obtaining written consent of the subjects. This study could have implications for cancer therapies.
Recent studies have shown that the SATB1 gene is a major regulator of numerous functions in the body, including the expression of various genes. This gene has also been linked with resistance to treatment in various kinds of cancer. While SATB1 has not been identified as a key component in nasopharyngeal carcinoma It has been linked to drug resistance in breast cancer. The expression of SATB1 has been evaluated using western blot analysis and reverse transcription-quantitative PCR.
The RNAi treatment slowed the growth of NPC cells that were treated with chemotherapy. The knockdown of SATB1 reduced the growth and invasion. Additionally, the RNAi treatment resulted in a reduction of E-cadherin and Vimentin. This has significant implications regarding cancer and drug resistant diagnosis. Inhibiting SATB1 could stop cancer cells developing drug resistance. The elimination of SATB1 could stimulate drug responses and reduce drug resistance.
Boster Bio SATB1 caused a decrease in cell viability in cells with 5-8F/DDP (and 5-8F/R), which were resistant to drugs and radiation. Additionally, SATB1 expression was decreased after the silencing of SATB1, while MMP-9 expression was increased. These results suggest that SATB1 could be a potential therapeutic target for cancerous cells.
SATB1 is a gene in the nuclear genome that is linked to radiation resistance in cancer cell cells. Eliminating SATB1 reduces the proliferation of NPC cells and their ability to infiltrate and spread. The SATB1 knockdown also reduces levels of E-cadherin, Vimentin. The SATB1 knockdown also inhibits the growth and spread of cancerous cells. These results suggest that knocking down SATB1 could prevent the growth of cancer.
SATB1 plays a role in many cellular processes as well as the expression of many genes. It has been linked to resistance to various cancers, but it is unclear whether SATB1 plays a role in the resistance to radiation in nasopharyngeal cancer. The 5-8F/R cell type was also developed. Expression of SATB1 was determined by reverse transcription-quantitative PCR (RT-qPCR) and western blot analysis.
PMID: 1505028 by Dickinson L.A., et al. A tissue-specific MAR/SAR DNA-binding protein with unusual binding site recognition.
PMID: 9111059 by Dickinson L.A., et al. An atypical homeodomain in SATB1 promotes specific recognition of the key structural element in a matrix attachment region.