Renalase Antibodies

Renalase (RNLS)

Catalyzes the oxidation of the abundant 1,2- dihydro-beta-NAD(P) and 1,6-dihydro-beta-NAD(P) to form beta- NAD(P)(+). The enzyme hormone is secreted by the kidney, and circulates in blood and modulates vascular function and systemic blood pressure.

Lowers blood pressure in vivo by decreasing cardiac contractility and heart rate and preventing a compensatory increase in peripheral vascular tone, suggesting a causal connection to the increased plasma catecholamine and heightened cardiovascular risk. High levels of catecholamines trigger plasma renalase and promotes its secretion and synthesis.

Gene Information

Human
Gene Name:	RNLS
Uniprot:	Q5VYX0
Entrez:	55328

Family

Belongs to:
renalase family

Alternative Names

C10orf59; C10orf59chromosome 10 open reading frame 59; EC 1.4; FLJ11218; MAO-C; Monoamine oxidase-C; Renalase; renalase, FAD-dependent amine oxidase; RNLS

Molecular Weight

Mass (kDA):
37.847 kDA

Genomic Context

Human
Location:	10q23.31
Sequence:	10; NC_000010.11 (88176052..88584480, complement)

Tissue Specificity

Secreted into the blood by the kidney. Highly expressed in the kidney, expressed at lower level in heart, skeletal muscle and small intestine. Its plasma concentration is markedly reduced in patients with end-stage renal disease, as compared with healthy subjects.

Subcellular Localizations

Secreted.

Diseases

• Diabetes Mellitus
• Malignant Neoplasms
• Neoplasms
• Diabetes Mellitus, Insulin-dependent
• Malignant Neoplasm Of Breast
• Lymphatic Metastasis
• Mammary Neoplasms
• Hereditary Diseases
• Heart Failure
• Inflammatory Breast Carcinoma
• Cataract

• Hypertensive Disease
• Atrial Fibrillation And Flutter
• Cardiovascular Diseases
• Autoimmune Reaction
• Cerebrovascular Accident
• Dysequilibrium Syndrome

Pathways

• Localization

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

Boster Bio: Best Uses of the RNLS Marker

RNLS, or Rapid Nuclear Localization Signal, is a secretory RNA found in liver cells. It is known to inhibit mitochondrial dysfunction and increase cell viability when subjected to oxidative strain. Learn more about the RNLS mark. Boster Bio: Best Uses of The RNLS Marker

RNLS is a secretory amino acid

The secretory enzyme RNLS encodes a gene that encodes a secretory substance that is highly expressed by the pancreas. Some forms of pancreatic disease have poor outcomes because of high levels of RNLS. Quantitative Polymerase Chain reaction (qPCR), was used in the measurement of RNLS mRNA concentrations in tumor samples. These cDNA Arrays contained 182 samples from pancreatic, including adenocarcinomas.

Cancer is characterised by dysregulation in cell senescence, death, and cell senescence. Renalase, which is a secretory flavoprotein protects cells from ischemic as well as toxic cellular injury. Renalase signals via plasma membrane calcium ATPasePMCA4b and activates PI3K/AKT/MAPK. It also plays an important part in cell-cycle regulation.

The inhibition of RNLS signaling induces apoptosis and arrests the cell cycle in Panc1 cells. Inhibiting the RNLS gene may have therapeutic value in melanoma. FIG. 25A displays the images of FIG. FIG. 25A depicts the effects anti-RNLSsiRNAs had on Panc1 cells. The cells were transfected by siRNAs that were RNLS-specific or non-specific. After 96 hour, cells were examined using the WST-1 method.

RNLS inhibits STAT3 signals in cancer cells. RNLS treatment of Panc1 cell lines inhibits STAT3 phosphorylation serine 727 and tyrosine 755. It also inhibits STAT3 activation. Anti-RNLS antibody inhibits tumor growth in a mouse xenograft. The anti-RNLS antibody m28RNLS (also known by 1D-28-4), inhibits the growth of tumor cells in vitro.

It is rich in antioxidant properties

Recent research shows that RNLS may have potent antioxidant properties. RNLS significantly decreased liver MDA augmentation and attenuated ROS production by t-BHP. It also increased liver SOD activity as well as liver GSH levels. These results indicate that RNLS may have antioxidant properties that could be beneficial in the treatment of liver IR injuries. These findings are subject to further investigation.

Exogenous RNLS at concentrations of 500 to 800 mM improved cell viability in hepatocytes under oxidative stresses. 500 mM was the ideal concentration for further experiments. The study also showed RNLS administration had a positive effect on cell viability in steatotic hepatocytes. RNLS treatment also decreased cyto C release and increased Bcl-2 transcription.

RNLS is a sensitive and responsive molecule to oxidative stresses. It specifically oxidizes the a-reducednicotinamide-adenine dinucleotide, NAD+ to b–NAD+. This is essential for energy metabolism and class III histone desacetylase activity. These results indicate that RNLS may be important in hepatic steatosis.

It inhibits mitochondrial dysfunction

Boster Bio's RNLS biomarker inhibits mitochondrial function of a variety of neuronal cells. These biomarkers might be useful in assessing mitochondrial functionality in vivo. However, they don't fully recapitulate the dynamics in different neuronal population populations. Additionally, the proliferation rates of various cell types, including PMBCs, alter mtDNA gene mutation loads. This further complicates the assessment for neuronal impairment using blood-based biomarkers.

Using a specific marker that can detect this process is a major step forward. While there are numerous approaches for treating Parkinson's disease, RNLS is one of the most effective and highly specific. In addition to detecting the presence of this protein, it also helps in predicting the effects of various therapeutic agents. Boster Bio's RNLS marker is able to accurately detect mitochondrial dysfunction because it can be caused by a variety factors.

Oxidative stress is a common side effect of mitochondrial dysfunction. Most compounds can influence both aspects mitochondrial dyshomeostasis. These compounds can improve bioenergetics by decreasing oxidative stress and decreasing Fe deposited. RNLS inhibitors are known to inhibit mitochondrial dysfunction in human cells. Boster Bio's RNLS Marker is aimed at reducing oxidative Stress.

Currently there is no FDA approved drug to prevent or reverse PD. However, it is becoming more apparent that mitochondria are essential to energy production and provide the fuel for life. A new drug that blocks mitochondrial dysfunction may provide a valuable therapeutic option in PD. Because of conflicting information and unknown pathophysiological function, pharmacokinetic assessment is not possible. If this is the case, it would be a welcome step toward treating the disease.

It improves cell viability in hepatocytes under oxidative stress

Boster Bio’s RNLS Marker, as previously reported, improved cell viability of hepatocytes through lowering MMP levels. L02 cells were subjected to different concentrations of H2O2 in order to study the effects on hepatic cell function. A western-blot assay was used for assessing cell viability.

RNLS significantly reduced oxidative damage in hepatocytes after exposure to t–BHP. The antioxidant properties of RNLS significantly reduced t-BHP induced ROS production and reduced MDA augmentation in liver cell cells. Supplementation of RNLS significantly reduced the levels of ALT/AST and LDH in steatotic mouse models.

RNLS is a crucial mediator of steatosis. Mice fed high-fat diets developed a fatty and enlarged livers. Despite this fatty liver condition RNLS administration significantly lowered IR damage, improved mitochondrial functioning, and increased hepatic lipid.

RNLS is a secreted protein. The serum level of RNLS decreased after HFD in mice. RNLS is essential for maintaining hepatocyte viability under oxidative stress. This study also demonstrated the anti-oxidative action of NAD+ in hepatocytes exposed to oxidative stresses.

RNLS is a well-known marker of hepatic redox health. This marker was created to increase cell viability in hepatocytes subjected to oxidative stresses. Biochemical analyses were performed in mice to measure serum levels of N-acetyltransferase, alanine aminotransferase, and LDH, which are indices of liver damage.

It is a promising therapeutic approach to attenuating liver injury from IR.

This study demonstrates that isoflurane preconditioning protects liver cells from primary hepatocyte injury and IR injury. The Laboratory of Animal Resources of Nanjing Medical University provided wild-type male C57BL/6 mouse models. All animals were provided with clean, safe environments and access to food and water. The Nanjing Medical University Institutional Animal Care and Use Committee reviewed the protocol.

This treatment also reduced hepatic IR injuries in mice by increasing hepatiocellular proliferative antiapoptosis. The increased LC3B II and p62 levels demonstrated the effects of ISO in liver autophagy. In a laboratory with primary hepatocytes, the treatment also decreased liver cell deaths. The therapy was well tolerated and can be used as a therapeutic strategy to reduce liver injury.