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- Table of Contents
1 Citations 5 Q&As
4 Citations 7 Q&As
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1 Citations 16 Q&As
Facts about Macrophage colony-stimulating factor 1.
Plays an essential role in the regulation of osteoclast proliferation and differentiation, the regulation of bone resorption, and is needed for normal bone development. Required for normal male and female fertility.
Human | |
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Gene Name: | CSF1 |
Uniprot: | P09603 |
Entrez: | 1435 |
Belongs to: |
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No superfamily |
colony stimulating factor 1 (macrophage); CSF1; CSF-1; Lanimostim; macrophage colony stimulating factor; macrophage colony-stimulating factor 1; MCSF; M-CSF; MCSFlanimostim; MGC31930
Mass (kDA):
60.179 kDA
Human | |
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Location: | 1p13.3 |
Sequence: | 1; NC_000001.11 (109910506..109930992) |
Cell membrane; Single-pass type I membrane protein.; [Processed macrophage colony-stimulating factor 1]: Secreted, extracellular space.
You might be wondering about the Best Uses of The CSF1 Markers. The answer to this question will differ according to the method employed. Let's discuss some of the methods, including Immunohistochemistry, ELISA, and Clinical applications. Once you've gained a basic understanding of the basics of each method, keep reading to learn more about what Boster Bio has in this area.
The ELISA for CSF1 detects the presence CSF1. This peptide is an essential component of the neurotransmitter BDNF. CSF1R is expressed in neurons, synapses and microglia. When mice lacking CSF1R have CAA and develop lower levels of adiponectin and other markers of cell death.
A suitable ELISA kit is required to detect an exact concentration of the peptide in cells. The standard curve includes three samples that have different levels of CSF1. With the standard curve the concentration of CSF1 in the sample can be calculated by analyzing the results. With a sandwich ELISA kit, three samples were tested 20 times for each concentration.
ELISA should include the p–aminobutyl–CoA internal standard for the CSF1 marker. This method detects the CSF1R in brain cells that are abundant in microglia. This gene also interacts with TREM2/b-Catenin and the IL-34 system and various other types of cells. Therefore, it could be useful to detect MS in human patients.
Recent research showed that mice treated with porcine CSF1Fc , a fusion protein, witnessed a significant increase blood monocytes, and tissue macrophages. Recombinant CSF1 was also extensively utilized in vitro to enhance the activity of monocytes, macrophages and macrophages. This suggests that CSF1 is an effective marker in MS.
An ELISA for the CSF1 marker uses sandwich enzyme-linked immuno-sorbent assay technology. After coating the antibody in the pre-coating phase with antigen biotin-conjugated reagents are then added to the wells. The entire plate is coated with an HRP-conjugated agent. The conjugates that are bound are removed by washing the buffer at each stage. The HRP enzymatic reaction can be measured by using a TMB substrate. The presence of CSF1 will result in a yellow-coloured layer on the plate.
In a study conducted by Dawson et al., ADGRE1 expression was elevated on pig alveolar macrophages. This was in line with the CSF1–Fc data. It was also observed in high concentrations on the pig liver where SIRP-alpha is present. These results show that CSF1 is an essential component of a healthy immune response.
The CSF1 Marker is an important protein that is made by bone marrow and plays an important role in regulating hematopoietic precursor cells. It also regulates the resorption of bone, cell adhesion and migration. It can be either a homodimer, heterodimer, or disulfide-linked one.
The CSF1R gene is a protein on the cell surface that plays a significant role in microglia. It also interacts with the IL-34 and TREM2/b-catenin signaling system and could be the reason for its beneficial effects on microglia growth. It was also shown that CSF1R deletion prevented cognitive impairment in APP mice that had been cKO.
The CSF1 marker is a new biomarker for cutaneous GVHD. CSF-1R, the receptor for CSF-1 is expressed by tissue-resident macrophages in cGVHD patients. CSF-1R inhibition of signaling could prevent cutaneous GVHD. It can also improve the outcome for cGVHD patients. This marker can also detect CSF-1R-deficient donor macrophages within cGVHD sufferers.
A variety of studies have proven that the expression of CSF-1 in tumor cells is linked to poor prognosis. Patients who have high levels of CSF-1 in their tumors are more likely suffer from distant metastasis and recurrence. CSF-1 expression was associated with higher rates of cancer recurrence in women suffering from uterine Sarcoma. Additionally, this biomarker has been demonstrated to predict the stage of the tumor, the presence of distant metastasis, and poor disease-free survival.
CSF-1 receptor inhibits tumor development by depleting B cells and preventing M2 macrophage invasion. The CSF-1R receptor is a key target in hematologic malignancies , as well as other diseases. Clinical applications of the CSF1 marker were recently published in Nat Med. More research is needed on this route to determine if it is a viable therapeutic strategy for patients with hematologic malignancies.
The CSF-1 biomarker can be useful in determining the extent to which skin rejection of the graft has occurred. Transplantation of donor cells could cause skin swelling and inflammation. In addition, CSF-1 treatment may worsen the cutaneous manifestations of chronic GVHD. One study found that mice lethally irradiated (B6 mice) received G-CSF-infused WT BAB/c (CD45.1) transplants. They also received either saline (10 mg/day) or CSF-1 (10mg/day) treatment. After day 14, mice who received CSF-1 or saline had significantly higher F4/80+ counts than control mice.
A CSF-1R inhibitor, PLX3397, inhibits monocyte differentiation. PLX3397 decreased the expression of CD163 and increased the expression of CD86 in M2 macrophages. The drug also decreased the expression of M2-like genes as well as increased the expression of genes that resemble M1. CSF-1R inhibition in vitro inhibits monocyte differentiation, which is the main reason why it is an effective CSF-1R antagonist.
The CSF1 marker is a crucial signaling molecule that controls many biological functions in human tissues. These include homeostasis of tissues as well as inflammation and repair of tissues. The capability to effectively target CSF1 or IL34 has been proven to be effective in regulating the differentiation of macrophages. In mice, CSF1R knockouts exhibit lower levels of macrophages, osteoclasts, as well as microglia.
The drug AFS98 and CSF1-Fc were given to patients with established acetaminophen-induced ALF. King's College Hospital validated the criteria used to assess patients. This was done to indicate their poor clinical condition and higher risk of death. Low levels of serum CSF1 levels were associated with liver transplantation, patient death and deterioration of the patient. The agents did not alter CYP2-mediated drug metabolism.
Dual blockade of IL34 and CSF1 reduced renal macrophages in mice. The drugs also reduced the expression of phagocytic hormones in liver cells. Dual blockade of CSF1 as well as IL34 reduced the amount of macrophages present in kidney tissues and was effective in halting the progress of lupus.
Serum levels of CSF1 were determined in patients with acute liver failure and compared to healthy controls. Two methods were employed to measure CSF1 one to compare the levels of patients suffering from acute liver diseases and the other to determine whether they responded to the medication. Researchers compared their results with those of healthy volunteers and patients suffering from acute liver failure. Patients whose CSF1 levels were below 25th percentile had liver failure.
CSF1 blockade in mice prevented the growth MC38 tumors using an animal model. The treatment reduced the number of tumor-infiltrating macrophages, as shown by the decrease in Ki67 staining. In addition, CSF1R-inhibition decreased tumor size by reducing the size of tumor foci. In addition it inhibited VE-cadherin expression and tumor vessel networks.
The peripheral monocytes whose function was inhibited by CSF1R returned to central nervous systems and suggest that peripheral monocytes are able to repopulate the central nervous system. This study has practical implications for the research results. Although CSF1R inhibition has important implications for human health, it's an ineffective biomarker. This is why CSF1R inhibition has attracted the attention it deserves. Therefore, it is important to comprehend its pharmacological significance.
PMID: 2996129 by Kawasaki E.S., et al. Molecular cloning of a complementary DNA encoding human macrophage- specific colony-stimulating factor (CSF-1).
PMID: 3493529 by Wong G.G., et al. Human CSF-1: molecular cloning and expression of 4-kb cDNA encoding the human urinary protein.
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