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- Table of Contents
4 Citations 8 Q&As
8 Citations 13 Q&As
2 Citations 7 Q&As
Facts about Inhibin beta A chain.
Inhibins appear to oppose the functions of activins. .
Human | |
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Gene Name: | INHBA |
Uniprot: | P08476 |
Entrez: | 3624 |
Belongs to: |
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TGF-beta family |
Activin A; activin AB alpha polypeptide; Activin beta-A chain; erythroid differentiation factor; Erythroid differentiation protein; follicle-stimulating hormone-releasing protein; FSH-releasing protein; inhibin beta A chain; inhibin beta A subunit; Inhibin, beta-1
Mass (kDA):
47.442 kDA
Human | |
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Location: | 7p14.1 |
Sequence: | 7; NC_000007.14 (41685101..41710532, complement) |
Secreted.
You're in the right spot if you're thinking of making use of INHBA to identify biomarkers. This protein can be used to determine the prognosis for cancer and the effects of various treatments. INHBA is also associated with tumor-infiltrating immune cells and regulates the M1/M2 polarization of macrophages.
Scientists have been studying the significance of INHBA in biomarkers for breast cancer over the recent years. It has been proven that the protein is expressed in tumors that are subsets of the tumor and could become a new therapeutic target. Researchers found that the protein's expression was associated with better prognosis, as well in a higher treatment effect. The study was conducted in mice and was confirmed by the results of xenograft mice studies.
Inhibin beta A is a member of the TGF family of proteins that are located in the nucleus of the cell and is synthesized in the cytoplasm, and secreted through the cell membrane. The overexpression of INHBA is associated with poor prognosis in cancer. The expression of this gene is related to the stage of metastasis from tumor lymph nodes. This suggests that INHBA could serve as a biomarker of treatment effect and prognosis in CRC. Researchers used microarrays to analyze data from CRC and human cells that had been killed. Then they conducted enrichment analysis to uncover functional networks.
The study also looked into the relationship between INHBA expression and the infiltration of immune cells within cervical cancer. The TCGA database contained 306 patients diagnosed with cervical cancer. The single-sample gene enrichment analysis (GSVA), R package was used to analyse INHBA's expression. They employed Spearman's rank correlation as well as Wilcoxon rank sum to evaluate the expression of INHBA with immune cell infiltration. The authors established p = 0.05 for the association between INHBA and immune cell infiltration.
While INHBA expression has increased in human esophageal cancer tissues, its function in adipose tissues is not yet understood. In mice, however, INHBA deletion results in a Cleft palate and absence of lower incisors. In addition, mice with type IIA activin receptors have a diminished reproduction.
A recent study has proved that INHBA can be a biomarker that could indicate treatment effects. The study has shown that knockdown of the protein by siRNA is 70% effective when compared to mock controls. A 10nM siRNA was used to inhibit the INHBA. It reduced proliferation by 5%, and 10 percent, respectively, over the time of 96 hours. INHBA can be used as a biomarker in prognosis and treatment effectiveness for cancer patients.
In a recent research, INHBA was discovered to be expressed in 46 different esophageal tissue samples. INHBA expression was found be anywhere from two to four times greater in 11 of the 15 samples than BM. In addition, two out of seven patients with HGD had two-fold or more INHBA expression compared to BM tissue. We also confirmed the results using real-time RTPCR.
In addition to these two types of cells, INHBA is also involved in the process of immune infiltration. In addition to being overexpressed, it is also a crucial regulator of cellular senescence and immune checkpoint ligands in CRC. These studies suggest that INHBA could be a biomarker for prognosis and treatment effects in CRC patients.
We identified the most INHBA-like genes using a GEPIA database of protein sequences. We also identified a conserved site of the miRNA family INHBA, as well as various functional categories connected to cellular components multicellular organisms, molluscans and multicellular organisms. These pathways are linked to the biological process that INHBA is involved with.
We also conducted single-sample enrichment studies of cervical cancer samples to further investigate the relationship between INHBA expression and immune cell infiltration. We also used Wilcoxon rank-sum test and Spearman's rank correlation tests to examine the association between INHBA expression and infiltration of immune cells. P-values were set to 0.05. The tumors showed significantly higher levels of INHBA expression than normal cells.
We have also discovered that reducing INHBA expression can inhibit the growth of cancerous gastric cells via the TGF-b signaling pathway. We also discovered that interfering with INHBA expression hindered gastric cancer growth by reducing cell proliferation, invasion, and migration. We also found that patients with MPM with high levels of INHBA had a lower prognosis. Patients could live longer with INHBA levels that are lower.
INHBA was associated with tumor-infiltrating immune cells within the PPI network. It was associated with the levels of infiltrating immune cells in CRC tumor samples. It also was linked to immune checkpoints, ligands, and immune checkpoints. INHBA expression also varied between normal and tumor samples. It is crucial to note that INHBA expression correlates with immune infiltration and progression of tumors.
We also observed that INHBA strongly correlated with immune infiltration, which includes T cells. This is significant because T cells are essential for evasion of the immune system. This protein was linked to multiple T cell biomarkers and common immune checkpoints. We also found that INHBA was abundantly expressed in human CRC tissues, cell lines and in a few cells. However the levels decreased after the death of a small portion of the cell. Therefore, INHBA is a new marker for immune cells that infiltrate tumors however further research is needed.
INHBA and JAG2 are two genes that are associated with high levels of expression in immune cells that invade tumors. The two genes have greater expression in tumors of the T-stage than normal tissues, suggesting that these two proteins might play a role in the progression of HNSCC. This research could have significant implications in future studies on HNSCC. Numerous new discoveries have been made which will to guide future research in this area of tumor immunotherapy.
In addition to being a member of the TGF superfamily, INHBA is encoded in the nucleus of the cell. It is synthesized in cytoplasm and secreted through the membrane. The overexpression of INHBA is associated with poor prognosis in cancer and could be an independent prognostic factor for intestinal cancers. To identify co-expression genes in HNSCC, the researchers used the KEGG pathway analysis and GO annotations.
Macrophages are ubiquitous immune cells, which play significant roles in the process of inflammatory. They also perform anti-inflammatory, wound healing, and bactericidal functions. They have two distinct characteristics, the M1 as well as the M2 and play a role in immune system polarization. The polarization response can be controlled by neuronal control.
In a recent study we discovered that activin A influences the gene-expression profile of M1 macrophages. Additionally that, anti-activin A antibodies abolish the transactivation capability of M1 macrophage-conditioned media. Activin A regulates the expression and function of a variety of genes involved in M1/M2-type Polarization.
We utilized gray histograms to assess gene expression. The expression of INHBA in macrophages of M2 is greater than that of M1 cells. However, under other conditions when there is a polarization shift in one direction, it could still be a sign there is an overall inflammatory change that is taking place. These findings aren't conclusive.
A genome-wide analysis also revealed novel osteolytic particle-induced mediators. Signaling pathways analysis also suggested that toll-like receptors as well as nod-like receptors are involved in recognition of the particles. Inflammatory response induced by titanium particles is influenced by the state of macrophage polarization. The inflammation response can be reduced by limiting M1 macrophage activity and promoting M2 polarization.
Inducible expression of the INHBA-encoded activin A (INHBA) in M1 macrophages is controlled by GM-CSF. It has also been established that activin A interferes with several M1 and IL-4 gene expressions. The anti-activin A antibody also blocks the acquisition of M1 markers by macrophages. The anti-activin A treatment did not affect the expression of the previously-identified activin A target gene, but it significantly enhanced SERPINE1 RNA. M1 macrophages release activin A more than M2 macrophages.
The study was the first to report distinct changes in the transcriptome of cardiac macrophages over the course of MI. This framework allows future studies to examine distinct macrophage subpopulations at every point in time. The study concluded that, although there was less variation in macrophages when they were pooled however, the number of genes within Cluster 3 was significantly greater than the total cells.
PMID: 3754442 by Mason A.J., et al. Structure of two human ovarian inhibins.
PMID: 3267209 by Murata M., et al. Erythroid differentiation factor is encoded by the same mRNA as that of the inhibin beta A chain.
*More publications can be found for each product on its corresponding product page