The kit takes out from the refrigeration should be balanced 15-30 minutes in the room temperature, if the coated ELISA plates have not been used up after opening, the plate should be stored in sealed bag.
Washing buffer will Crystallization separation, it can be heated the water helps dissolve when dilution. Washing does not affect the result.
Pipette sample with pipettors each step, and proofread its accuracy frequently, avoids the experimental error. Pipette sample within 5 min, if the number of sample is much, recommend using multichannel pipettor.
If the testing material content is excessively high (The sample OD is higher than the first standard well)?please dilute sample (n-fold).
Adhesive Strip only limits the disposable use to avoid cross-contamination.
The substrate should be preserved evade the light.
Please refer to use instruction strictly. The test result determination must take the microtiter plate reader as a standard.
All samples, washing buffer and each kind of reject should refer to infective material process.
Do not mix reagents with those from other lots.
Reactivity : Pig
Method type : Sandwich ELISA
Minimum Detection Limit :
Detection Range :
Application : ELISA
Purpose : For the quantitative determination of target substances concentrations.
Research Area : Tags & Cell Markers->Cell Type Markers->Tumor Associated, Signal Transduction->Cytoskeleton / ECM->Cell Adhesion->Cell Adhesion Molecules->Vascular, Signal Transduction->Cytoskeleton / ECM->Cell Adhesion->Cell Adhesion Molecules->Endothelial, Neuroscience->Neurology process->Neural Signal Transduction, Stem Cells->Mesenchymal Stem Cells->Surface Molecules, Cancer->Invasion/microenvironment->ECM->Cell adhesion->Other, Cardiovascular->Atherosclerosis->Vascular Inflammation->Leukocyte recruitment->Cell adhesion molecules, Kits/ Lysates/ Other->Kits->ELISA Kits->ELISA Kits->Adhesion molecules ELISA kits, Kits/ Lysates/ Other->Kits->ELISA Kits->ELISA Kits->Atherosclerotic proteins ELISA kits, Cardiovascular->Angiogenesis->Endothelial Cell Markers
Sample Type : serum, plasma, Urine, tissue samples, cell culture supernates
Plate : Pre-coated,Strips (12 x 8)
Restrictions : For Research Use only
Storage : 2 °C – 8 °C
Storage Comment : Store at 4°C for 6 months, at -20°C for 12 months. Avoid multiple freeze-thaw cycles
Expiry Date : 12 months
Size : 96T
Immunogen : Synthetic peptide conjugated to KLH derived from within residues 350 – 450 of Human GDF 5.
Availability : 3-5 working days
Target Details : Could be involved in bone and cartilage formation. Chondrogenic signaling is mediated by the high-affinity receptor BMPR1B.Predominantly expressed in long bones during embryonic development.Defects in GDF5 are the cause of acromesomelic chondrodysplasia Grebe type (AMDG). Acromesomelic chondrodysplasias are rare hereditary skeletal disorders characterized by short stature, very short limbs, and hand/foot malformations. The severity of limb abnormalities increases from proximal to distal with profoundly affected hands and feet showing brachydactyly and/or rudimentary fingers (knob-like fingers). AMDG is an autosomal recessive form characterized by normal axial skeletons and missing or fused skeletal elements within the hands and feet.Defects in GDF5 are the cause of acromesomelic chondrodysplasia Hunter-Thompson type (AMDH). AMDH is an autosomal recessive form of dwarfism. Patients have limb abnormalities, with the middle and distal segments being most affected and the lower limbs more affected than the upper. AMDH is characterized by normal axial skeletons and missing or fused skeletal elements within the hands and feet.Defects in GDF5 are the cause of brachydactyly type C (BDC). BDC is an autosomal dominant disorder characterized by an abnormal shortness of the fingers and toes.Defects in GDF5 are the cause of Du Pan syndrome (DPS); also known as fibular hypoplasia and complex brachydactyly. Du Pan syndrome is a rare autosomal recessive condition characterized by absence of the fibulae and severe acromesomelic limb shortening with small, non-functional toes. Although milder, the phenotype resembles the autosomal recessive Hunter-Thompson and Grebe types of acromesomelic chondrodysplasia.Defects in GDF5 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 GDF5 are the cause of multiple synostoses syndrome type 2 (SYNS2). Multiple synostoses syndrome is an autosomal dominant condition characterized by progressive joint fusions of the fingers, wrists, ankles and cervical spine, characteristic facies and progressive conductive deafness.Defects in GDF5 are a cause of brachydactyly type A2 (BDA2). Brachydactylies (BDs) are a group of inherited malformations characterized by shortening of the digits due to abnormal development of the phalanges and/or the metacarpals. They have been classified on an anatomic and genetic basis into five groups, A to E, including three subgroups (A1 to A3) that usually manifest as autosomal dominant traits.Genetic variations in GDF5 are associated with susceptibility to osteoarthritis type 5 (OS5). Osteoarthritis is a degenerative disease of the joints characterized by degradation of the hyaline articular cartilage and remodeling of the subchondral bone with sclerosis. Clinical symptoms include pain and joint stiffness often leading to significant disability and joint replacement.Defects in GDF5 may be a cause of brachydactyly type A1 (BDA1). Brachydactylies (BDs) are a group of inherited malformations characterized by shortening of the digits due to abnormal development of the phalanges and/or the metacarpals. They have been classified on an anatomic and genetic basis into five groups, A to E, including three subgroups (A1 to A3) that usually manifest as autosomal dominant traits.
Precision : Intra-assay Precision (Precision within an assay) CV%<15% Three samples of known concentration were tested twenty times on one plate to assess. Inter-assay Precision (Precision between assays) CV%<15% Three samples of known concentration were tested in twenty assays to assess.
Linearity : To assess the linearity of the assay, samples were spiked with hig3h concentrations of rat ADP in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.
Typical Data : These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed. ng/ml OD1 OD2 Average 1000 0.088 0.090 0.089 500 0.135 0.142 0.139 250 0.227 0.237 0.232 125 0.324 0.341 0.333 62.5 0.583 0.598 0.591 31.25 0.847 0.864 0.856 15.62 1.228 1.235 1.232 0 2.155 2.199 2.177