TFAP2C Antibodies

Transcription factor AP-2 gamma (TFAP2C)

Sequence-specific DNA-binding protein which interacts with inducible viral and cellular enhancer elements to regulate transcription of selected genes. AP-2 factors bind to the consensus sequence 5'-GCCNNNGGC-3' and activate genes involved in a large spectrum of important biological functions including proper eye, face, body wall, limb and neural tube development.

They also suppress a number of genes including MCAM/MUC18, C/EBP alpha and MYC. Involved in the MTA1-mediated epigenetic regulation of ESR1 expression in breast cancer.

Gene Information

Human
Gene Name:	TFAP2C
Uniprot:	Q92754
Entrez:	7022

Family

Belongs to:
AP-2 family

Alternative Names

Activating enhancer-binding protein 2 gamma; AP2 gamma; AP-2 gamma; AP2-GAMMA; ERF1; estrogen receptor factor 1; hAP-2g; TFAP2C; TFAP2G; transcription factor AP-2 gamma (activating enhancer binding protein 2 gamma); transcription factor AP-2 gamma (activating enhancer-binding protein 2 gamma); transcription factor AP-2 gamma; Transcription factor ERF-1

Molecular Weight

Mass (kDA):
49.177 kDA

Genomic Context

Human
Location:	20q13.31
Sequence:	20; NC_000020.11 (56629306..56639283)

Subcellular Localizations

Nucleus.

Diseases

• Malignant Neoplasms
• Neoplasms
• Malignant Neoplasm Of Breast
• Carcinoma
• Mammary Neoplasms
• Cell Transformation, Neoplastic
• Malignant Paraganglionic Neoplasm
• Carcinoma In Situ
• Crest Syndrome
• Testicular Neoplasms
• Neoplasms, Germ Cell And Embryonal
• Choriocarcinoma
• Embryonal Carcinoma

• Seminoma
• Germ Cell Tumor
• Carcinogenesis
• Tumor Progression
• Neoplasm Metastasis
• Teratoma
• Nervousness

Interacting Proteins

• CITED2
• UBE2I

Pathways

• Methylation
• Cell Differentiation
• Oncogenesis
• Gastrulation
• Dna Methylation
• Cell Growth
• Pathogenesis
• Spermatogenesis
• Cell Cycle
• Cell Development
• Localization
• Germ Cell Development
• Transport

• Response To Camp
• Stem Cell Maintenance
• Cell Cycle Arrest
• Reverse Transcription
• Histone Acetylation
• Cholesterol Transport
• Placenta Development

PTMs

• Methylation
• Cleavage
• Sumoylation

• Demethylation
• Deacetylation
• Acetylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/TFAP2C

Best Uses Of The TFAP2C Marker

This page will help you find a TFAP2C marker to use in your experiments. This protein coding gene can be expressed in fibroblasts. It's used to amplify all known mouse Psg genes. This article will explain the function and uses of this marker. You should also know a few important things before you purchase the antibody.

TFAP2C can be described as a protein-coding gene

The expression of TFAP2C in colorectal cancer is a highly variable event that correlates with poor prognosis in patients and disease progression. TFAP2C, which is upregulated in colorectal tumour cells, increases spheroids development and inhibits apoptosis. However, downregulation restores chemotherapeutic sensitivity. TFAP2C promotes stemness in colorectal tumor cells by blocking the Hippo signaling pathway.

TFAP2C belongs to the activating proteins 2 family. It encodes a transcription element known as AP-2 gamma. It is found within the decidu and in the chorion of mammals. It has been implicated for many types of tumors. Both the human and mouse mammary cells express the TFAP2C protein. TFAP2C levels in mice are higher than those in humans.

It is not clear what role TFAP2C may play in lung carcinoma. Studies have shown that TFAP2C may be involved in tumorigenesis via EGFR gene expression. TFAP2C may also be a cause of EGFRTKI-resistant lung carcinoma. lncRNAs involved in TFAP2C-regulated pathways may be key participants in the mechanisms of EGFR-TKI resistance in lung cancer.

TFAP2C interacts directly with Myc and KDM5B through distinct domains located in their Cterminal regions. Overexpression of any one of these proteins led to S-phase entry and decreased checkpoint activation. In addition, each protein has been implicated in poor prognosis in breast cancer. TFAP2C (a protein coding genes that promotes tumourigenesis) is one example.

By inhibiting CDK activity, p21cip acts as a regulator of cell-cycle progression. It is essential for activation of G1/S and G2/M checkspoints. Overexpression of TFAP2C reduced the cytostatic effects of HU, vinblastine, as well as increasing the percentage of cells in S-phase. Interestingly, KDM5B was not overexpressed, but it increased CDKN1A repression by TFAP2C.

Branchiooculofacial disorder is caused by mutations in the AP2-gamma genetic. It is characterized as abnormalities of the neck, face, and eyes. Complete knockout or deletion of the TAP2C genes disrupts their activity as corepressors. It also causes embryonic/fetal mortality. This gene is closely associated with AP2-gamma, making it crucial to ensure that cells develop as normal.

It is expressed within fibroblasts

TFAP2C, a transcription factor, has been implicated in somatic cells reprogramming as well as naive pluripotency. Although it is not clear how it regulates somatic cells reprogramming, it's important to understand. It is known that overexpression of Tfap2c promotes mesenchymal-to-epithelial transition and inhibits c-Myc-dependent apoptosis.

TFAP2C contains a helix loop-helix DNA binding domain that specifically binds with the GC rich consensus sequence in DNA. This domain is responsible TFAP2C's transcriptional activity. It is found in many fibroblasts. It has been linked to several solid tumors. It is involved in angiogenesis in melanoma. It also increases expression of epidermal grow factor receptors, leading to increased proliferation, and tumor growth.

TFAP2C expression is also found in human fibroblasts. TFAP2C was identified by this study as a direct target for many genes. These genes include genes which are important for the epiblasts as well as genes that affect pre-implantation embryos. We also identified a number TFAP2C/ lines. The same transfection procedure was used to create the TFAP2C/ line and a Control Line 1. The murine ESCs were plated at 150 k/well, and harvested using trypsin & precipitate.

TFAP2C plays an important role in maintaining pluripotency. It is also expressed in the morula before blastocyst formation. It could therefore be used in order to reset the chromatin landscape before artificial systems in vitro of in vitro regression naive pluripency. It is thought that it plays a key role in embryonic human development.

The progression of cancer has been linked to TFAP2C levels. To determine if it plays a role in the development NSCLC, further research will be needed. The role of TFAP2C as a regulator of lung tumorigenesis is still unclear. Although there are many important functions for TFAP2C it is still not clear. It may be necessary, to detect lung cancer earlier, to use a biomarker.

The TFAP2C protein co-activator PELP1 is required for TFAP2C to function. It acts as a coregulator to several NRs. PELP1 has an histone-binding area that recognizes histone variations and interacts well with chromatin-modifying components. RNA-seq analysis using a BC cell-line revealed 318 genes that were PELP1-regulated. Interestingly, many of these genes are involved in BC progression.

TFAP2C may be involved in activation of target loci and repression. It can only exert its influence on promoters if it exists. The enrichment in AP2 motifs demonstrates its important role for gene regulation. TFAP2C is also known to interact with the CITED family of proteins, and it recruits the histone acetyltransferase p300 to enhance enhancers.

It is used for amplifying all known mouse Psg sequences

We used high-throughput sequencing technology to clone mice genomes to test the hypothesis Psg gene was a receptor for progesterone. We designed primer sets that corresponded to the Hprt gene in mouse Psg genes. Using an ABI PRISM 7900 sequence detection system, we performed quantitative PCR using a qPCR kit from Applied Bio-systems. The qPCR mastermix contains Amplitaq (r).

Quantitative RTPCR was used to determine transcript levels of mouse Psg gene within spongiotrophoblasts. Primers were used in order to amplify the N domains of all known mouse Psg genetics. The concentration of the primers has been optimized to minimize nonspecific amplification. The lowest threshold cycles and primer sets of 300 pmol have been identified. PCR-based dissociation graphs revealed a single peak for each of the genes.

The TFAP2C amplification process was originally created to determine the relative transcription level of mouse Psg genetics. The method was then modified so that six litters of mRNA were used. This amplify technique was able to identify Psg gene transcription levels in placentas between E8.5 and E18.

CD9 can also occur in the uterus. CD9 is known reduces the amount Psg available for interaction to maternal immune cells. However, further research is needed to determine if there is any interaction between Psg and CD9, despite the widespread expression. CD9, if Psg has been expressed in the uterus is the surrogate for the null mutant.

The amplify method offers many benefits. For one thing, TFAP2C is highly efficient in generating PCR products that amplify all known mouse Psg gene sequences. Moreover, the Psg protein itself is located on the cell surface of the endothelium and the mesometrial pole. This makes Psg protein secreted by the fetus can be associated with the maternal vascular endothelium. A pregnant woman is also likely to experience a lot of angiogenesis and vascular remodeling. The trophoblast gigantic cells produce a wide variety of antiangiogenic and angiogenic compounds.

TFAP2C and EOMES are expressed in trophoblast cells of mice and humans. Their interactions depend on the relative abundance of their components. ELF5 recruits TFAP2C into triply-occupancy locations in mouse Psg gene sequences. These proteins then trigger binding with the Tfap2c cognate motif.