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- Table of Contents
Facts about PR domain zinc finger protein 14.
May play a vital role in germ cell development at two levels: the reacquisition of potential pluripotency, including SOX2 up-regulation, and effective epigenetic reprogramming, characterized by EHMT1 repression. Its association with CBFA2T2 is needed for the functions in pluripotency and germ cell formation (By similarity).
Human | |
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Gene Name: | PRDM14 |
Uniprot: | Q9GZV8 |
Entrez: | 63978 |
Belongs to: |
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class V-like SAM-binding methyltransferase superfamily |
MGC59730; PFM11; PR domain containing 14; PR domain zinc finger protein 14; PR domain-containing protein 14; PRDM14; PR-domain zinc finger protein 14
Mass (kDA):
64.062 kDA
Human | |
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Location: | 8q13.3 |
Sequence: | 8; NC_000008.11 (70051613..70071252, complement) |
Expressed in embryonic stem cells. Tends to be overexpressed in breast cancer (at protein level).
Nucleus.
This article discusses the functions and associations of Boster’s PRDM14 Marker with polycomb complex 2 as well as breast cancer benefits. For scientists, continue reading! Boster scientists also have the option to submit their research for product credit. This article is applicable worldwide to all scientists. You can also submit results related to your species, application, or special samples.
The PRDM14 marker is an important component of epigenetic remodeling in germ cell lineages. It controls distinct aspects of epigenetic reprogramming in the vivo. We know little about the spatial distribution of epigenetic reprogramming in germ cells. PRDM14 is necessary for the polycomb-associated H3K27me3 marking. PRDM14 are required for the maintenance and synthesis of the H3K27me3 Mark.
PRDM14, a regulator protein, binds with the introns Xist and upstream of Xist activater Rnf12. It facilitates repression of Xist during the cytokinesis-dependent reprogramming process (XCR). H3K27me3 is not removed from the X chromosome. This is Xist-dependent. PRDM14, on the other hand, promotes global DNA-demethylation via passive dilution.
PRDM14 is an essential regulator for germ cell fate in mammals, but its role is not clear in deuterostomes. In fact, it is possible that PRDM14 might need to be reexamined for its role in deuterostomes. The diversity of Prdm14 expression is dependent on the mode of germ cell specification, which comprises preformation and epigenesis. Extrinsic signals are used to induce germ cells from pluripotent cell lines in deuterostomes.
PRDM14 is an essential regulator of transcriptional repression of ESCs. It also interacts with polycomb repressor compound two (PRC2). Although there has not been any evidence of interaction between PRDM14 (PRC2) and PRDM14, some studies do suggest it. H3K27me3 enrichment and PRDM14-binding region levels decrease in mESCs that are deficient in PRDM14.
By binding to genes that control cell type switching, the Prdm14 marker plays an essential role in the maintenance of pluripotent stem cell lines. Prdm14 absence results in the death of mouse pluripotent cells. They also lose their ability for pluripotency maintenance and become incapable of dividing into reproductive stem cells. Prdm14 contains a SET domain that binds to genes involved in the maintenance of pluripotent stem cells. Although Prdm14 does not switch on genes, it is believed to play a part in pluripotency.
Mb(S14), an innovative tool to disrupt Prdm14 activity in live cells, is called Mb(S14). These researchers have also used this protein in studies to study gene expression and pluripotency. This innovative tool could also open the door to Prdm14 targeting in cancers. It may be possible, in the end to determine the most efficient use of this particular protein. Prdm14 being a central component in the ESC could be beneficial for the study and analysis of cancer-related pluripoency.
RNA-seq data from mutant Prdm14 proteins should be accompanied by a heatmap or PCA analysis. While GO term are important for analyzing data on gene expression, heatmaps should also include information regarding multiple mutants' RNA-seq results. Data should be correlated with mESC biology.
Monobodies are of interest to all and can be used in place of mouse Prdm14. This protein has a SETdomain that is similar in structure to human PRDM12.
The current study tested Prdm14 monoclonal anti-Mtgr1 antibodies. This protein plays an important part in germline growth and pluripotency. These antibodies can be used for testing the druggability and interaction between Mtgr1 and PRDM14. The Mb(S4) binds to a distinct surface of Prdm14, which inhibits PGC-LC induction.
This study also found that bEPSCs cultured on chemical-fixed MEFs maintained their pluripotency. MEFs cultivated on methanol fixed MEFs maintained their pluripotency in a similar manner. MT–bEPSCs displayed higher levels fatty acid de Novo synthases, indicating that these cells possess similar metabolic properties to MC–MEFs.
The presence H3K27me3 chromatin marks is required for the repressive functionality of Polycomb repressor complicated 2 (PRC2). This mark is introduced by the PRC2 core complex, which includes EED, SUZ12, NuRF55, and Rbap46/48. PRC2 also includes a variety proteins, including JARID2, AEBP2, EED and SUZ12, as well as JARID2.
Polycomb repressor compound 2 (PRC2) mediates the chromatin reorganization process and promotes gene suppression. Point mutations in individual subunits of the complex have been linked to tumorgenesis. While there are several inhibitors targeting PRC2, the molecular mechanism underlying their recognition remains largely elucidated. Ciferri's team did however describe the structure of the protein compounds and have solved two crystal structures.
The Polycomb regulatory complex is a family of chromatin modification enzymes. It plays an important part in cell-type identification and development. Its methyltransferase activity in H3K27 cells chromatin defines its repressive mode. PRC2 dysfunction is also linked to cancer. However, various mechanisms modulate its activity. H3K27me3 stimulates polycomb activity. Dense chromatin, however, inhibits PRC2. Different accessory subunits also regulate the activity of PRC2 in various ways.
PRDM14, which is a zinc finger protein, is a potential therapeutic target. It is also implicated in HPV-induced cervical tumors. Methylation-mediated PRDM14 gene suppression offers a new therapeutic target. Similar to 5-azacytidine in that it inhibits the growth and development of tumor cells, cisplatin alters methylation.
PMID: 17942894 by Nishikawa N., et al. Gene amplification and overexpression of PRDM14 in breast cancers.
PMID: 20953172 by Chia N.Y., et al. A genome-wide RNAi screen reveals determinants of human embryonic stem cell identity.