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- Table of Contents
Facts about Plexin-C1.
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Human | |
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Gene Name: | PLXNC1 |
Uniprot: | O60486 |
Entrez: | 10154 |
Belongs to: |
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plexin family |
CD232 antigen; CD232; plexin (semaphorin receptor); Plexin C1; PLXNC1; PLXN-C1; receptor for viral semaphorin protein; receptor for virally-encoded semaphorin; VESPR; VESPRplexin-C1; Virus-encoded semaphorin protein receptor
Mass (kDA):
175.742 kDA
Human | |
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Location: | 12q22 |
Sequence: | 12; NC_000012.12 (94148577..94307675) |
Detected in heart, brain, lung, spleen and placenta.
Membrane; Single-pass type I membrane protein.
This article will help you find a new biomarker. This article will cover the best uses of PLXNC1 in a variety situations: Clinical applications, Biological assays and combinations with other marks. Boster Bio was founded in 1993 by Steven Boster, a man who gained notoriety as "he who converts science in the lavatory".
PLXNC1 is an alveolar space protein that influences the infiltration and tissue dysfunction of neutrophils. PLXNC1 inhibition may alter the levels both in the lung and in the BAL compartments. Anti-PLXNC1-treated mice showed significantly lower levels for cytokine mRNAs in the lungs as well as the BAL.
Anti-PLXNC1 antibody led to a decrease in PLXNC1 gene expression in a mouse model of lung cancer. This resulted in fewer lung histological changes. Moreover anti-PLXNC1 proteins inhibited the growth in mice of a bacterial strain. These results support a hypothesis PLXNC1 hyperexpression could be a cause of fibrosis.
Lung injury was caused by PLXNC1. Inhibiting the protein significantly reduced inflammation in the lungs and improved survival rates. It also reduced the severity of pulmonary injury, and it helped to reduce inflammation. Further, interference with PLXNC1 may provide new therapeutic approaches in the future. While the PLXNC1 peptide might be a promising drug candidates, it will take years for its validity to be confirmed.
The expression of PLXNC1 in lungs of ventilated mice has also been confirmed. Moreover, PLXNC1 is induced in pulmonary epithelial cells in response to acute inflammation. Its promoter region is bound to NF-kB and PLXNC1 becomes positive after stimulation with TNF-a. This gene is also associated IL-6 is released, which can cause lung injury.
PLXNC1 can be described as an oncogene which regulates cell proliferation and apoptosis. We validated the PLXNC1 marker using the GEPIA online databank. The Kaplan Meier Plotter was also used to assess the prognostic power of PLXNC1 in melanoma patients.
To confirm these findings, we measured PLXNC1 expression in STAD specimens to confirm them. This protein was significantly increased in STAD samples than GAPDH. We also found that PLXNC1 expression in STAD patients was significantly higher than in patients who had no disease. We also found that STAD patients with PLXNC1 expression was associated with poor outcomes compared with healthy controls. Our study also confirmed the results by studying different groups of STAD patients, based on their race or number of lymph nodes.
Biological tests using the PLxNC1 gene marker are useful in detecting expression of this gene across different tissues. The marker can be used to detect miR-4500 a smallRNA involved gene expression. This marker can be used with a variety of primers, including the human PLXNC1 primer. The primers used for this study were created to detect miR-4500, and the PLxNC1 genes.
The immune-related IRF5 gene regulates the PLXNC1 protein. The expression of this gene in cancer cells significantly correlated with the M2 macrophage population, a biomarker for a poor outcome in patients with stomach adenocarcinoma. It has been demonstrated that this gene has significant regulatory connections with other immune cell types.
Multiple databases found expression of PLXNC1 within tumor cells. STAD samples showed higher levels of the protein than did normal tissues, and patients with STAD had poorer prognosis. The LinkedOmics database identified significant differences in STAD patients and normal controls. STAD patients had a T stage and a pathological stage that were different. The number of lymph nodes, race, and tumor cell type were all important factors in determining PLXNC1 expression.
PLXNC1 has an affinity for miR-4500. This was useful in detecting miR-4500. Cells were harvested using cell-lysis buffer containing protease inhibition cocktail and RNase inhibitor to determine if miR-4500 bound PLXNC1. After incubating cells, the tubes were shaken for 1 hours at 30°C.
Nanoparticles can be used in bioassays for many reasons. However, this technology has some limitations. First, there are a large number of bioassays based on the use of NPs. Second, there can be a number of drawbacks to NPs that make them useless in bioanalysis. These disadvantages are not meant to hinder research.
Cross-reactivity among antibodies is a limitation to the use NPs as immunoassays. These limitations can be overcome by NPs, which allow simultaneous determination of multiple compounds. Numerous recent examples have shown that NPs can be useful in multiplexed analyses. Multiplexed assays is the current trend. The PLXNC1 molecule is a promising choice for simultaneous determinations many molecules.
Recent research has shown that PLXNC1 may play a role in lung injury. Researchers used a transgenic mouse to study PLXNC1 in bronchoalveolar saline after ventilation at 15 and 45 mbar. Combinations with other PLXNC1 markers can also help identify pulmonary diseases. Here are some examples of combinations with other PLXNC1 markers.
Molecular and Functional Specialization of GPR182, MEIS2, and C-MAF. We identified a set of regulated genes in vitro using LSECs derived from HUVECs as well as Pro-LGMN. This was done by Western blotting along with immunostaining. These markers were detected in the same blots. We also performed a DAVID analysis to determine the expression of individual PLXNC1. The results are summarized in Table 1.
PMID: 9586637 by Comeau M.R., et al. A poxvirus-encoded semaphorin induces cytokine production from monocytes and binds to a novel cellular semaphorin receptor, VESPR.
PMID: 20727575 by Liu H., et al. Structural basis of semaphorin-plexin recognition and viral mimicry from Sema7A and A39R complexes with PlexinC1.