Serum amyloid A-1 protein Antibodies

Serum amyloid A-1 protein (SAA1)

Major acute phase protein. .

Gene Information

Human
Gene Name:	SAA1
Uniprot:	P0DJI8
Entrez:	6288

Family

Belongs to:
SAA family

Alternative Names

Serum Amyloid A1

Molecular Weight

Mass (kDA):
13.532 kDA

Genomic Context

Human
Location:	11p15.1
Sequence:	11; NC_000011.10 (18266225..18269977)

Tissue Specificity

Expressed by the liver; secreted in plasma (at protein level).

Subcellular Localizations

Secreted.

Diseases

• Amyloidosis
• Inflammation
• Arthritis
• Rheumatoid Arthritis
• Secondary Amyloidosis
• Acute-phase Reaction
• Familial Mediterranean Fever
• Brucellosis
• Malignant Neoplasms
• Liver Carcinoma
• Plaque, Amyloid
• Neoplasms

• Kidney Diseases
• Amyloid Deposition
• Carcinoma
• Amyloid Nephropathy
• Liver Neoplasms
• Inflammatory Response
• Cardiovascular Diseases

Pathways

• Pathogenesis
• Inflammatory Response
• Acute-phase Response
• Immune Response
• Translation
• Localization
• Secretion
• Amyloid Fibril Formation
• Transport
• Proteolysis
• Cell Adhesion
• Tissue Remodeling
• Cholesterol Efflux

• Lipid Binding
• Cell Cycle
• Mrna Stabilization
• Methylation
• Cytokine Production
• Cell Activation
• T Cell Activation

PTMs

• Cleavage
• Nitration

• Phosphorylation
• Methylation

• Glycosylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/SAA1

Best Uses of the SAA1 Marker

The serum amyloid A1 marker an enzyme that is made by the liver and circulates through the blood. Its purpose is unclear, but it appears to play an important role in the immune system, helping to repair damaged tissue and acting as an antibacterial agent. It also serves as a signal to the migration of germ-fighting cells. This article will give an overview of the SAA1 signal and its applications.

The physiological functions

The SAA1 marker is multifunctional molecule that controls multiple signaling pathways. It is involved in cell proliferation and survival and plays a significant role in the regulation of apoptosis and inflammation. The receptors for SAA activate NF-kB by interfacing with TLRs and RAGE. SAA stimulates multiple signaling pathways that are anti-apoptotic and proinflammatory. It is also involved in the remodeling of tissues and wound healing.

The mRNA that is responsible for SAA3 is present in a small fraction of mammary epithelial cell populations of bovine. It is expressed in modest amounts during pregnancy and at low levels during lactation. However, it reaches its highest levels during involution. The mature SAA3 protein has been demonstrated to possess antibacterial properties. Molenaar and colleagues speculated that SAA3 could protect the gastrointestinal tract of a newborn baby.

The activation of SAA1 has been proven to stimulate nitric-oxide production, suggesting that SAA1 stimulates the M1 subset. This was confirmed by an increase in NF-kB activation as well as releases of cytokine. The SAA1 molecule facilitates the development of a M1-like subset of macrophages. While the results of these studies are limited, it is clear that SAA1 is essential for the development of a healthy immune system.

Patients who have high levels of SAA1 are at risk of a poor prognosis. Additionally, it has been demonstrated to inhibit angiogenesis and metastasis of tumors. SAA1 also regulates ERK signaling an ERK signaling pathway that is connected to inflammation and immune reactions. It is related to the development of malignant transformations as well as cell migration.

The activation of SAA1-AF488 produced an increase in macrophage metabolic activity as determined by the presence of the luciferase substrate. However, polymyxin B neutralizes the LPS-induced increase in macrophage metabolism. Polymyxin B neutralized the effects of SAA1 on macrophages however, it did not affect apoptotic cells.

Predictive value

A recent study has demonstrated that the serum SAA concentrations are a highly effective marker for the detection of poststroke infection. The study also showed that the serum SAA levels were strongly linked to renal function and were the strongest indicator of mortality for patients suffering from AA amyloidosis. In addition, the findings suggest that SAA is a novel marker for poststroke infections. Additionally, the results suggest the importance of SAA in further investigation and monitoring closely of this subgroup. These findings could be used to assist healthcare professionals identify patients with a high risk of infection and avoid unnecessary antibiotic treatment.

Although the absence of SAA1 gene expression does not significantly affect the growth of a tumor, it does reduce its prognostic value. The absence of Saa3 expression may play a role in the development of tumors. Additionally, Saa1 has been found to be highly expressed in Adipocytes. These findings could point to a potential therapeutic target for cancer patients. Researchers hope to continue their research into the role of SAA1 in pancreatic cancer.

The study also demonstrated that SAA is associated with the endoscopic findings of patients with ulcerative colitis. It is better than CRP in predicting. Additionally, it is more useful in predicting the occurrence of endoscopic activity in UC patients who are clinically remission. The authors of the study Danese S and Colombel JF discovered that the early endoscopic diagnosis of UC is associated with better clinical outcomes than symptoms that develop later.

It is interesting to know that high SAA1 expression is associated with poor survival in patients who have low levels of stroma. So, if SAA1's overexpression correlates with a worse prognosis in patients with low stroma, it is likely that this protein plays as a dual function tumor cells and stroma. Researchers are also developing treatments for cancer patients who have SAA1.

The SAA1 protein functions as an ortholog to the Saa3 molecule. Poor prognosis is related to SAA1 in patients suffering from RA. Its presence in blood is also an excellent indicator of a poor outcome for PDAC patients. Nevertheless, it is important to examine the underlying mechanism behind the association between SAA1 expression and RA. The effects of SAA1 on prostate health aren't known.

Limitations

The SAA1 protein was found to bind to numerous Gram-negative bacteria. It also induces responses in neutrophils (cells responsible for killing invading pathogens) and macrophages (cells responsible for rapid killing). The SAA1 marker binds to bacteria in a manner similar to the immune response to normal human blood serum, which is expected to contain immunoglobulin. It binds to bacteria which may opsonize it, such as Shigella flexneri or Vibrio cholerae. However, SAA does not bind to bacteria that aren't in the process of being opsonized by the immune system.

This marker is not 100% sensitive. The SP and SE concentrations could be very different. SAA1 concentrations may not be reliable for diagnosing clinical conditions. However, the ratio SAA1/SAA2 was used to identify patients at risk of developing infections. Patients who contracted infections had an incidence ratio of 0.97 to those who did not. These results indicate that SAA1 is highly sensitive and specificity.

Further research is required to confirm the results of the SAA1 study and its predictive value. The SAA/SAA2 marker need to be validated in a larger population with enough samples for subgroup analysis. It is possible that SAA concentrations should be combined with other clinical scales in order to increase the accuracy of this association. In the end, it is essential to be aware of the limitations of the SAA1/SA2 marker.

In the present study, SAA1 was identified with a mouse recombinant, which lacks LPS. It was found to be at the best concentration for the study, which is the most accurate reflection of the pathogenesis and physiology behind amyloidogenesis. Other factors that contributed to the study were polymyxin B and staurosporine. The authors have declared no conflict of interest and appreciate the co-authors for their help and cooperation in the study of the SAA1 marker.

Another drawback of the SAA1 marker is that the chi-square test only comprises SAA1 exons one three and four. Furthermore, this test does not take into account other factors that might affect blood pressure and other medical conditions. Doctors can still determine whether the SAA1 marker is correct by using a high-quality panel which includes M1-related genes. This research could lead to more precise diagnosis.

Source

While the precise function of SAA1 remains unclear It is believed that it could play a significant role in the estimation radiation doses in humans. Its synthesis occurs primarily in the liver, making it a promising biomarker of lethality in mice. It was also observed in patients suffering from nasopharyngeal carcinoma and in people exposed to radiation.

It isn't yet clear the causes of SAA-mediated bone loss. While the exact mechanism is not yet understood, SAA binds bacteria products and may influence bone loss in live. However, SAA is an important mediator of inflammation that contributes to osteoporosis. Inflammation is a major cause of dental caries, and SAA plays an important role in regulating these processes.

Researchers tested antiserums against human SAA1 to determine whether it was expressed in the human body. The antiserums tested had the titer higher than 1:500. Boster bio's SAA1 marker does not bind to a particular isoform of the molecule, but it binds both the HDL lipoproteins as well as the lipoproteins apoAI.

The anti-SAA1 protein has the ability to be a phospholipid binder at different pH levels. This effect has not been documented in previous studies. Therefore, further research is needed to understand the mechanism of the pH-dependent interactions between apolipoproteins and PC. This article focuses on the role of SAA1 in controlling the phospholipid content of the human body. Once we have a better understanding of the mechanism of SAA-mediated interactions with phospholipids, it is possible to further identify the mechanisms responsible for SAA-mediated aggregation.

The role of SAA1 in the immune response in humans is not fully comprehended. However, researchers have shown that SAA1 increases in acute radiation illness. LPS is a major bacterial endotoxin can also cause SAA1 to be expressed by humans. The universal marker for bacteria is the 16S rRNA gene. It is used to identify them. It can be measured by Quantitative PCR.

While the role of SAA1 in the human disease is not yet clear however, it has been linked to immune responses that are inherently. It is created during inflammation and has potential for defending against infection. Infection-associated amyloid A is also believed to be a neutrophil-specific molecule. Human periapical lesion have high levels of SAA1 in their tissues. There is no evidence linking SAA1 to periodontitis.