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Human Noggin ELISA Kit (RMEK-0152819)

Cat. No.: RMEK-0152819

Category: ELISA Kits

INQUIRY 1 x 96 tests
Human Noggin ELISA Kit is a single-wash 90 min sandwich ELISA designed for the quantitative measurement of Noggin protein in serum and plasma. The technology employs capture antibodies conjugated to an affinity tag that is recognized by the monoclonal antibody used to coat our plates. This approach to sandwich ELISA allows the formation of the antibody-analyte sandwich complex in a single step, significantly reducing assay time.

Product Features

Species Reactivity Human
Detection Method Colorimetric
Assay Duration One step assay
Assay Time 1.5 h
Assay Type Sandwich (quantitative)
Precision Intra-Assay-Serum-8-4.9%; Inter-Assay-Serum-3-8.3%
Sensitivity 11 pg/mL
Range 54.7 pg/mL - 3500 pg/mL
Sample Type Cit plasma, EDTA Plasma, Serum
Recovery Serum-83-80% - 85%; EDTA Plasma-85-83% - 88%; Cit plasma-88-82% - 93%
Key Features One-wash 90 minute protocol; Sensitivity: 11 pg/mL; Range: 54.7 pg/mL - 3500 pg/mL; Sample type: Cit plasma, EDTA Plasma, Serum; Detection method: Colorimetric; Assay type: Sandwich (quantitative); Reacts with: Human

Target Information

Target Symbol NOG
UniProt ID Q13253
Biomarker of SCs/CSCs Hepatic Cancer
Function Essential for cartilage morphogenesis and joint formation. Inhibitor of bone morphogenetic proteins (BMP) signaling which is required for growth and patterning of the neural tube and somite.
Cellular Localization Secreted.
Involvement in Disease Defects in NOG are a cause of symphalangism proximal syndrome (SYM1). SYM1 is characterized by the hereditary absence of the proximal interphalangeal (PIP) joints (Cushing symphalangism). Severity of PIP joint involvement diminishes towards the radial side. Distal interphalangeal joints are less frequently involved and metacarpophalangeal joints are rarely affected whereas carpal bone malformation and fusion are common. In the lower extremities, tarsal bone coalition is common. Conducive hearing loss is seen and is due to fusion of the stapes to the petrous part of the temporal bone. Defects in NOG are the cause of multiple synostoses syndrome type 1 (SYNS1); also known as synostoses, multiple, with brachydactyly/symphalangism-brachydactyly syndrome. SYNS1 is characterized by tubular-shaped (hemicylindrical) nose with lack of alar flare, otosclerotic deafness, and multiple progressive joint fusions commencing in the hand. The joint fusions are progressive, commencing in the fifth proximal interphalangeal joint in early childhood (or at birth in some individuals) and progressing in an ulnar-to-radial and proximal-to-distal direction. With increasing age, ankylosis of other joints, including the cervical vertebrae, hips, and humeroradial joints, develop. Defects in NOG are the cause of tarsal-carpal coalition syndrome (TCC). TCC is an autosomal dominant disorder characterized by fusion of the carpals, tarsals and phalanges, short first metacarpals causing brachydactyly, and humeroradial fusion. TCC is allelic to SYM1, and different mutations in NOG can result in either TCC or SYM1 in different families. Defects in NOG are a cause of stapes ankylosis with broad thumb and toes (SABTS); also known as Teunissen-Cremers syndrome. SABTS is a congenital autosomal dominant disorder that includes hyperopia, a hemicylindrical nose, broad thumbs, great toes, and other minor skeletal anomalies but lacked carpal and tarsal fusion and symphalangism. Defects in NOG are the cause of brachydactyly type B2 (BDB2). BDB2 is a subtype of brachydactyly characterized by hypoplasia/aplasia of distal phalanges in combination with distal symphalangism, fusion of carpal/tarsal bones, and partial cutaneous syndactyly.

Storage & Shipping

Storage Store at 2-8°C
Shipping Gel Packs
Stability The stability of kit is determined by the loss rate of activity. The loss rate of this kit is less than 5% within the expiration date under appropriate storage condition.

For research use only. Not for clinical use.