Rabbit anti-Human NOG Polyclonal Antibody | anti-NOG antibody

NOG (Noggin) (HRP)

Cat. Num. AAA6387242

• Gene Names: NOG; SYM1; SYNS1; SYNS1A
• Reactivity: Human
• Applications: Western Blot
• Purity: Purified by Protein A Affinity Chromatography.
• Synonyms: NOG; Polyclonal Antibody; NOG (Noggin) (HRP); anti-NOG antibody

• Host: Rabbit
• Reactivity: Human
• Clonality: Polyclonal
• Isotype: IgG
• Specificity: Recognizes human NOG.
• Purity/Purification: Purified by Protein A Affinity Chromatography.
• Form/Format: Supplied as a liquid in PBS, pH 7.2. No preservative added. Labeled with Horseradish Peroxidase (HRP).
• Sequence Length: 1913

• Applicable Applications for anti-NOG antibody: Western Blot (WB)
• Application Notes: Applications are based on unconjugated antibody.
• Immunogen: Full length human NOG, aa1-232 (NP_005441.1)
• Immunogen Sequence: MERCPSLGVTLYALVVVLGLRATPAGGQHYLHIRPAPSDNLPLVDLIEHPDPIFDPKEKDLNETLLRSLLGGHYDPGFMATSPPEDRPGGGGGAAGGAEDLAELDQLLRQRPSGAMPSEIKGLEFSEGLAQGKKQRLSKKLRRKLQMWLWSQTFCPVLYAWNDLGSRFWPRYVKVGSCFSKRSCSVPEGMVCKPSKSVHLTVLRWRCQRRGGQRCGWIPIQYPIISECKCSC
• Conjugate: HRP
• Note: Preservative Free
• Preparation and Storage: Store product at 4 degree C if to be used immediately within two weeks. For long-term storage, aliquot to avoid repeated freezing and thawing and store at -20 degree C. Aliquots are stable at -20 degree C for 12 months after receipt. Dilute required amount only prior to immediate use. Further dilutions can be made in assay buffer. Note: Sodium azide is a potent inhibitor of peroxidase and should not be added to HRP conjugates. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Western Blot (WB)

(NOG rabbit polyclonal antibody. Western Blot analysis of NOG expression in human liver.)

Western Blot (WB)

(NOG rabbit polyclonal antibody. Western Blot analysis of NOG expression in Jurkat.)

Western Blot (WB)

(Western Blot analysis of NOG expression in transfected 293T cell line by NOG polyclonal antibody. Lane 1: NOG transfected lysate (25.8kD). Lane 2: Non-transfected lysate.)

Related Product Information for anti-NOG antibody

Noggin is a 232aa containing secreted protein belonging to the noggin family. Cartilage morphogenesis and joint formation are some of the functions of Noggin. It also acts as an 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), multiple synostoses syndrome 1 (SYNS1), tarsal-carpal coalition syndrome (TCC) and stapes ankylosis with broad thumb and toes brachydactyly type B2 (BDB2). It shows a restricted expression in few brain parts and uterus.

Product Categories/Family for anti-NOG antibody

Antibodies; Growth Factors; Cytokines

NCBI and Uniprot Product Information

• NCBI GI #: 1732746295
• NCBI GeneID: 9241
• NCBI Accession #: NM_005450.6
• NCBI GenBank Nucleotide #: NM_005450
• UniProt Accession #: Q13253
• NCBI Official Full Name: Homo sapiens noggin (NOG), mRNA
• NCBI Official Synonym Full Names: noggin
• NCBI Official Symbol: NOG
• NCBI Official Synonym Symbols: SYM1; SYNS1; SYNS1A
• NCBI Protein Information: noggin
• UniProt Protein Name: Noggin
• Protein Family: Noggin
• UniProt Gene Name: NOG
• UniProt Entry Name: NOGG_HUMAN

NCBI Description

The secreted polypeptide, encoded by this gene, binds and inactivates members of the transforming growth factor-beta (TGF-beta) superfamily signaling proteins, such as bone morphogenetic protein-4 (BMP4). By diffusing through extracellular matrices more efficiently than members of the TGF-beta superfamily, this protein may have a principal role in creating morphogenic gradients. The protein appears to have pleiotropic effect, both early in development as well as in later stages. It was originally isolated from Xenopus based on its ability to restore normal dorsal-ventral body axis in embryos that had been artificially ventralized by UV treatment. The results of the mouse knockout of the ortholog suggest that it is involved in numerous developmental processes, such as neural tube fusion and joint formation. Recently, several dominant human NOG mutations in unrelated families with proximal symphalangism (SYM1) and multiple synostoses syndrome (SYNS1) were identified; both SYM1 and SYNS1 have multiple joint fusion as their principal feature, and map to the same region (17q22) as this gene. All of these mutations altered evolutionarily conserved amino acid residues. The amino acid sequence of this human gene is highly homologous to that of Xenopus, rat and mouse. [provided by RefSeq, Jul 2008]

Uniprot Description

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

Chromosomal Location of Human Ortholog: 17q22

Cellular Component: extracellular space; extracellular region

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

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

Disease: Stapes Ankylosis With Broad Thumb And Toes; Symphalangism, Proximal, 1a; Brachydactyly, Type B2; Multiple Synostoses Syndrome 1; Tarsal-carpal Coalition Syndrome