Aquaporin-1 Antibodies

Aquaporin-1 (AQP1)

Forms a water-specific channel that offers the plasma membranes of red cells and kidney proximal tubules with high permeability to water, thereby permitting water to move in the direction of an osmotic gradient. .

Gene Information

Human
Gene Name:	AQP1
Uniprot:	P29972
Entrez:	358

Family

Belongs to:
MIP/aquaporin (TC 1.A.8) family

Alternative Names

28-kDa; AQP1; AQP-1; AQP-CHIP; aquaporin 1 (channel-forming integral protein, 28kDa); aquaporin 1 (Colton blood group); Aquaporin 1; Aquaporin-CHIP; CHIP28; CHIP2828kDa, CO blood group); CO; MGC26324

Molecular Weight

Mass (kDA):
28.526 kDA

Genomic Context

Human
Location:	7p14.3
Sequence:	7; NC_000007.14 (30911853..30925516)

Tissue Specificity

Detected in erythrocytes (at protein level). Expressed in a number of tissues including erythrocytes, renal tubules, retinal pigment epithelium, heart, lung, skeletal muscle, kidney and pancreas. Weakly expressed in brain, placenta and liver.

Subcellular Localizations

Cell membrane; Multi-pass membrane protein.

Diseases

• Edema
• Neoplasms
• Disease Of Adrenal Medulla
• Diabetes Mellitus
• Malignant Neoplasms
• Brain Edema
• Tumor Angiogenesis
• Nervousness
• Carcinoma
• Kidney Diseases
• Nephrogenic Diabetes Insipidus
• Salivary Gland Diseases

• Pulmonary Edema
• Polyuria
• Lung Injury
• Neoplasm Metastasis
• Pathologic Neovascularization
• Fibrosis
• Inflammation

Interacting Proteins

• CCDC36
• CCDC57
• CEP44
• CRTAC1
• CSRNP1

• FSD2
• IKZF2
• IKZF3
• KCTD9
• KIAA1958

• KRT31
• KRT33B
• KRT40
• KRTAP10-7
• KRTAP4-2

• KRTAP9-2
• MDFI
• MTUS2
• NOTCH2NL
• RGS17

• RGS20
• RIMBP3
• SIAH1
• SPRY2
• TCF4

• TNK2
• TRAF1
• TRAF2
• TRIM23
• TRIP6

Pathways

• Transport
• Water Transport
• Localization
• Secretion
• Water Homeostasis
• Fluid Transport
• Angiogenesis
• Excretion
• Cell Migration
• Pathogenesis
• Cellular Localization
• Cell Proliferation
• Glycosylation

• Glycerol Transport
• Reverse Transcription
• Glomerular Filtration
• Rna Interference
• Exocytosis
• Translation
• Wound Healing

PTMs

• Phosphorylation
• Glycosylation
• Cleavage
• Ubiquitination
• Deglycosylation
• Biotinylation
• Demethylation

• Nitrosylation
• Amidation
• Decarboxylation
• Dephosphorylation
• Reduction
• Oxidation
• Methylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/AQP1

Best Uses Of The AQP1 Marker

Like the name suggests, this biomarker is a potential therapeutic target for acute kidney injury (AKI). It has been proven that the AQP1 gene regulates NFKB and activation of NFKBa and may reduce the inflammatory response. This marker can be used by researchers to analyze AKI as well as other conditions. Here are the top applications of this biomarker.

The AQP1 gene is a possible therapeutic target for AKI

Sepsis is a serious condition that causes an abnormal response to infection, and a high rate of mortality (17 17 %). Sepsis is the most frequent cause of AKI in critically ill patients. It is responsible for more than half of all cases in the intensive care unit. Recent research has proven that circulating endothelial cells (EV) have a significant role in AKI and sepsis. EVs might play a major role , not only in inflammation but also in AKI.

In the event of sepsis the kidneys lose the ability to concentrate water, leading to AKI. The AQP1 channel is found in the plasma membranes of endothelial cells in the outer medullary descending vasa recta. It is responsible for controlling the flow of water across cell membranes. The targeted disruption of AQP1 in mice has been demonstrated to reduce the ability of concentration of the urinary tract. Knockout mice had lower basal urine osmolality, and higher levels of polyuria. Vasopressin administration and starvation reduced the maximum urinary osmolality.

Recent studies have identified a variety of biomarkers of kidney injury caused by ischemia. The urinary exosomes contain a high concentration in fetuin A, activating the transcription factor 3 as well as aquaporin-1. These biomarkers can aid in early detection of AKI patients, thereby improving treatment strategies. A growing body of research is looking into Fetuin A as a potential therapeutic target for AKI.

EVs can deliver interleukin-10 while also inhibiting expression of IL-10. This makes them a promising candidate to alter IL-10 levels in AKI patients. While these findings are encouraging but there is a long way to go before human trials. The absence of early indicators of predictive value has made treatment implementation of targeted EV therapy very difficult. AKI is a difficult condition, and the lack of a reliable biomarker can cause problems in the treatment process.

A variety of primary antibodies were utilized in this study. Primarily antibodies against CD63 as well as integrin A-L and CD81 were employed. Abcam also used an anti-RFP antibody ab186873.

It is essential to detect AKI early. Early detection of CKD is essential to prompt initiation of antihypertensive therapies and to prevent the progression to ESRD. In addition to the higher chances of recovery and survival being diagnosed early, early detection of CKD can allow patients to get the most effective treatment and avoid the condition from progressing to chronic kidney disease.

It reduces the inflammation response through p38 MAPK

Recent research has shown that vicenin 3, the compound known as vicenin 3 blocks the degrading of extracellular matrix which is an important aspect of OA. The compound also blocks p38 MAPK signals. Both total p38 and p-p38 were determined by western blot analysis. The secretion of MMPs' proteins, aggrecan, and collagen type II were also measured by using an ELISA kit.

The results showed that serum levels of AQP1-5-9 had been significantly decreased in the lung. The effects were more evident in the ileum. The results also suggest that AQP1 reduces inflammation through p38 MAPK. In conclusion, the findings of this study suggest that Boster Bio AQP1 reduces the inflammation response via the MAPK p38.

Furthermore, TRPM2 silencing significantly attenuated the inflammatory response in mice with diabetes induced by STZ or HFD. These effects were mediated by inhibitions of the TGF-b1-activated JNK1 pathway. The results suggest that Boster Bio AQP1 can reduce inflammation via MAPK p38 and reduces production of cytokine.

Moreover, it inhibited the LPS-induced inflammation in human mesothelial cells in the peritoneal. Additionally, it blocked the expression of ERK1/2 and PPARg in these cells. It also blocked expression of pro-inflammatory mediators inside RAW264.7 cells. This suggests that the substance's sugar content is a significant determinant of its anti-inflammatory properties.

Arctium Lappa L. is an vitamin K3 analog reduces inflammation through inhibiting NF-IoB expression. Aloin can inhibit lipopolysaccharide-induced caspase-3 and apoptotic cells and inhibits NF-IoB signaling.

The compound also inhibited the expression of iNOS, and also slowed the activation of the MAPK pathway JNK/p38. Mangiferin also blocked the phosphorylation by LPS of TLR2 or TLR4 receptors. Furthermore, it suppressed the nuclear translocation of NFIoB p65 and blocked its binding to DNA. Furthermore, mangiferin inhibited phosphorylation of STAT1 and the MAPK p38. These results suggest the possibility for this compound to be employed as a treatment option for periodontitis.

It blocks the activation of the NF-kB/IkBa pathway

Boster Bio AQP1 is an additive to decrease NF-kB activity. It inhibits the phosphorylation IkBa which is a major transcription factor in the nuclear. IkBa is phosphorylated when it is stimulated by LPS and then translocates into the nucleus. It activates a wide range of genes once it's there.

Inflammation occurs the process where cells lose the ability to regulate their own internal environment. Fluid regulation is a vital aspect of cell physiology and the loss of it can lead to a dramatic change in the cell's physiology. Typical inflammation features include swelling of cells and tissue swelling known as oedema. AQP1 could regulate water transport and inflammasome activity. However, AQP1 does not appear to be an effective inhibitor of inflammation.

TRIM67, a negative regulator that blocks the activation of NF-kB is a new compound. The compound inhibits the activation of NFkB by inhibiting TNFa. TRIM67 interacts to the degron motif S110 of NF-kB. By inhibiting TNFa-dependent NF-kB, it can suppress cancer-causing cells and inhibit inflammatory processes.

AQP1 is an all-natural supplement that has multiple uses. It inhibits the activation of the NFKB/IkBa pathway and reduces the NFKB/IkA signaling causcade. It also blocks p65's binding to the kappa-B site in DNA.

This supplement is a natural substance that has a proven track record of anti-inflammatory properties. Its effectiveness in reducing inflammatory cytokines in humans is backed by clinical studies. Boster Bio AQP1 slowed down the activation of the IkBa/NFKBa pathway. It has also been demonstrated to be effective in treating multiple inflammatory disorders.

The company has confirmed Boster Bio AQP1 Antibody to be used in Flow Cytometry. The antibody is able to bind Rat, Mouse, and Human. It is highly specific and blocks activation of the NFKB/IkBa pathway. In addition, it blocks the production of inflammation-related cytokines in cancer cells.