Overview

  • Product name

    LVV Hemorphin 7 ELISA kit
  • Detection method

    Colorimetric
  • Precision

    Intra-assay
    Sample n Mean SD CV%
    LVV Hem 7 20 708.1pg/ml 4.1%
    LVV Hem 7 20 305.5pg/ml 8.8%
    LVV Hem 7 20 71.5pg/ml 20.9%
    Inter-assay
    Sample n Mean SD CV%
    LVV Hem 7 707pg/ml 9.2%
    LVV Hem 7 334.1pg/ml 9.5%
    LVV Hem 7 72.3pg/ml 16.5%
  • Sample type

    Serum, Tissue Extracts
  • Assay type

    Competitive
  • Sensitivity

    6.1 pg/ml
  • Range

    9.8 pg/ml - 10000 pg/ml
  • Recovery

    Sample specific recovery
    Sample type Average % Range
    Serum = 94 100ng/ml - 5000ng/ml
    Tissue Extracts = 95 100ng/ml - 5000ng/ml

  • Assay time

    3h 0m
  • Assay duration

    Multiple steps standard assay
  • Species reactivity

    Reacts with: Rat, Human
  • Product overview

    Abcam’s LVV Hemorphin 7 in vitro competitive ELISA (Enzyme-Linked Immunosorbent Assay) kit is designed for the accurate quantitative measurement of LVV Hemorphin 7 in serum and tissue homogenates. This kit it not intended for use with plasma samples.

    A polyclonal anti-Rabbit-IgG antibody has been precoated onto 96-well plates. Standards or test samples are added to the wells, along with a solution of LVV Hemorphin 7 conjugated to biotin, followed by a solution of polyclonal antibody to LVV Hemorphin 7. The plate is washed to remove unbound reagents. A solution of streptavidin-HRP conjugate is then added. After further incubation the excess reagents are washed away and TMB substrate is added, which is catalyzed by HRP to generate a yellow color. A stop solution changes this color from yellow to blue, and the intensity of this blue coloration is inversely proportional to the amount of LVV Hemorphin 7 captured in the plate.

  • Notes

    AnalyteSequencePercent cross reactivities in the range of 0.1 pM - 500 nM
    LVV Hemorphin 7LVVYPWTQRF100
    Leu-Valorphin-Arg (LVV Hemorphin-6)VVYPWTQR<0.003
    ValorphinVVYPWTQ<0.003
    Ang(1-12)DRVYIHPFHLVI<0.003
    Ang IDRVYIHPFHL<0.003
    Ang(1-9)DRVYIHPFH<0.003
    Ang IIDRVYIHPF<0.003
    Ang(1-7)DRVYIHP<0.003
    Ang AARVYIHPF<0.003
    Ang IIIRVYIHPF<0.003
    Ang IVVYIHPF<0.003
  • Tested applications

    Suitable for: Competitive ELISAmore details
  • Platform

    Microplate

Properties

  • Storage instructions

    Please refer to protocols.
  • Components 1 x 96 tests
    20X Wash Buffer Concentrate 1 x 27ml
    Assay Buffer 16 1 x 30ml
    Goat anti-rabbit IgG Microplate (12 x 8 wells) 1 x 96 tests
    HRP- Streptavidin Conjugate 1 x 12.5µg
    LVV Hemorphin 7 Antibody 1 x 6ml
    LVV Hemorphin 7 Conjugate 1 x 6ml
    LVV Hemorphin 7 Standard 2 x 40ng
    Plate Sealer 2 units
    Stop Solution 2 1 x 10ml
    TMB Substrate 2 x 10ml
  • Research areas

  • Function

    Involved in oxygen transport from the lung to the various peripheral tissues.
    LVV-hemorphin-7 potentiates the activity of bradykinin, causing a decrease in blood pressure.
  • Tissue specificity

    Red blood cells.
  • Involvement in disease

    Defects in HBB may be a cause of Heinz body anemias (HEIBAN) [MIM:140700]. This is a form of non-spherocytic hemolytic anemia of Dacie type 1. After splenectomy, which has little benefit, basophilic inclusions called Heinz bodies are demonstrable in the erythrocytes. Before splenectomy, diffuse or punctate basophilia may be evident. Most of these cases are probably instances of hemoglobinopathy. The hemoglobin demonstrates heat lability. Heinz bodies are observed also with the Ivemark syndrome (asplenia with cardiovascular anomalies) and with glutathione peroxidase deficiency.
    Defects in HBB are the cause of beta-thalassemia (B-THAL) [MIM:613985]. A form of thalassemia. Thalassemias are common monogenic diseases occurring mostly in Mediterranean and Southeast Asian populations. The hallmark of beta-thalassemia is an imbalance in globin-chain production in the adult HbA molecule. Absence of beta chain causes beta(0)-thalassemia, while reduced amounts of detectable beta globin causes beta(+)-thalassemia. In the severe forms of beta-thalassemia, the excess alpha globin chains accumulate in the developing erythroid precursors in the marrow. Their deposition leads to a vast increase in erythroid apoptosis that in turn causes ineffective erythropoiesis and severe microcytic hypochromic anemia. Clinically, beta-thalassemia is divided into thalassemia major which is transfusion dependent, thalassemia intermedia (of intermediate severity), and thalassemia minor that is asymptomatic.
    Defects in HBB are the cause of sickle cell anemia (SKCA) [MIM:603903]; also known as sickle cell disease. Sickle cell anemia is characterized by abnormally shaped red cells resulting in chronic anemia and periodic episodes of pain, serious infections and damage to vital organs. Normal red blood cells are round and flexible and flow easily through blood vessels, but in sickle cell anemia, the abnormal hemoglobin (called Hb S) causes red blood cells to become stiff. They are C-shaped and resembles a sickle. These stiffer red blood cells can led to microvascular occlusion thus cutting off the blood supply to nearby tissues.
    Defects in HBB are the cause of beta-thalassemia dominant inclusion body type (B-THALIB) [MIM:603902]. An autosomal dominant form of beta thalassemia characterized by moderate anemia, lifelong jaundice, cholelithiasis and splenomegaly, marked morphologic changes in the red cells, erythroid hyperplasia of the bone marrow with increased numbers of multinucleate red cell precursors, and the presence of large inclusion bodies in the normoblasts, both in the marrow and in the peripheral blood after splenectomy.
  • Sequence similarities

    Belongs to the globin family.
  • Post-translational
    modifications

    Glucose reacts non-enzymatically with the N-terminus of the beta chain to form a stable ketoamine linkage. This takes place slowly and continuously throughout the 120-day life span of the red blood cell. The rate of glycation is increased in patients with diabetes mellitus.
    S-nitrosylated; a nitric oxide group is first bound to Fe(2+) and then transferred to Cys-94 to allow capture of O(2).
    Acetylated on Lys-60, Lys-83 and Lys-145 upon aspirin exposure. PubMed:16916647 reports the identification of HBB acetylated on Lys-145 in the cytosolic fraction of HeLa cells. This may have resulted from contamination of the sample.
  • Information by UniProt
  • Alternative names

    • Beta globin chain
    • Beta-globin
    • CD113t C
    • HBB
    • HBB_HUMAN
    • Hemoglobin beta
    • Hemoglobin beta chain
    • Hemoglobin subunit beta
    • LVV-hemorphin-7
    see all
  • Database links

Applications

Our Abpromise guarantee covers the use of ab136942 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
Competitive ELISA Use at an assay dependent concentration.

Images

  • Representative Standard Curve using ab136942.

  • Dose‐response curves from human plasma and serum diluted into assay buffer were compared to the LVV Hemorphin 7 standard curve. The parallel response indicates the standard effectively mimics the native protein.

Protocols

References

ab136942 has not yet been referenced specifically in any publications.

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