Mouse Noggin (NOG) ELISA kit; SYM1; SYNS1; symphalangism 1 (proximal) ; noggin

For Research Use Only. Not for use in diagnostic procedures.

This assay has high sensitivity and excellent specificity for detection of Mouse NOG. No significant cross-reactivity or interference between Mouse NOG and analogues was observed.

Unopened test kits should be stored at 2 to 8 degree C upon receipt. Please refer to pdf manual for further storage instructions.

Manufactured in an ISO 13485:2003 and EN ISO 13485:2012 Certified Laboratory.

Select online data sheet information is drawn from bioinformatics databases, occasionally resulting in ambiguous or non-relevant product information. It is the responsibility of the customer to review, verify, and evaluate the information to make sure it matches their requirements before purchasing the kit. Our ELISA Kit assays are dynamic research tools and sometimes they may be updated and improved. If the format of this assay is important to you then please request the current manual or contact our technical support team with a presales inquiry before placing an order. We will confirm the current details of the assay. We cannot guarantee the sample manual posted online is the most current manual.

Small volumes of NOG elisa kit vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

MBS930943 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the noggin, ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing NOG. The ELISA analytical biochemical technique of the MBS930943 kit is based on NOG antibody-NOG antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect NOG antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, NOG. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

25,770 Da

noggin

noggin

Noggin

NOGG_MOUSE

NOG: 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. 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. Belongs to the noggin family.

Protein type: Secreted, signal peptide; Secreted

Cellular Component: extracellular space; extracellular region

Molecular Function: protein homodimerization activity; cytokine binding; protein complex binding

Biological Process: neural tube development; limb development; axon guidance; central nervous system development; wound healing; somatic stem cell maintenance; regulation of neuron differentiation; embryonic skeletal development; multicellular organismal development; regulation of BMP signaling pathway; motor axon guidance; middle ear morphogenesis; negative regulation of transcription from RNA polymerase II promoter; negative regulation of BMP signaling pathway; BMP signaling pathway; notochord morphogenesis; cell differentiation in hindbrain; ureteric bud development; negative regulation of cardiac muscle cell proliferation; axial mesoderm development; anatomical structure formation; negative regulation of osteoblast differentiation; cell differentiation; negative regulation of cell migration; skeletal development; neural plate morphogenesis; in utero embryonic development; pattern specification process; osteoblast differentiation; negative regulation of cell differentiation; mesenchymal cell differentiation; mesoderm formation; dorsal/ventral pattern formation; endoderm formation; spinal cord development; pituitary gland development; cartilage development; negative regulation of astrocyte differentiation; neural tube closure; epithelial to mesenchymal transition; positive regulation of transcription from RNA polymerase II promoter; brain development; embryonic digit morphogenesis; urogenital system development; positive regulation of epithelial cell proliferation

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