Human VAPB (Vesicle-associated membrane protein-associated protein B/C) ELISA Kit | VAPB elisa kit

Human VAPB (Vesicle-associated membrane protein-associated protein B/C) ELISA Kit

Cat. Num. AAA7612210

• Gene Names: VAPB; ALS8; VAP-B; VAMP-B
• Reactivity: Human
• Synonyms: VAPB (Vesicle-associated membrane protein-associated protein B/C); Human VAPB (Vesicle-associated membrane protein-associated protein B/C) ELISA Kit; Vesicle-associated membrane protein-associated protein B/C; VAMP-B/VAMP-C; VAMP-associated protein B/C; VAP-B/VAP-C; UNQ484; PRO983; VAPB; VAPB elisa kit

• Reactivity: Human
• Specificity: This assay has high sensitivity and excellent specificity for detection of VAPB. No significant cross-reactivity or interference between VAPB and analogues was observed.

• Samples: Serum, plasma, tissue homogenates and other biological fluids
• Assay Type: Quantitative Sandwich
• Detection Range: 31.25-2000pg/ml
• Sensitivity: 18.75pg/ml
• Intra-assay Precision: CV<8%
• Inter-assay Precision: CV<10%
• Preparation and Storage: Store at 2-8 degree C for 6 months

Typical Testing Data/Standard Curve (for reference only)

Related Product Information for VAPB elisa kit

Principle of the Assay: This kit was based on sandwich enzyme-linked immune-sorbent assay technology. Capture antibody was pre-coated onto 96-well plates. And the biotin conjugated antibody was used as detection antibodies. The standards, test samples and biotin conjugated detection antibody were added to the wells subsequently, and washed with wash buffer. HRP-Streptavidin was added and unbound conjugates were washed away with wash buffer. TMB substrates were used to visualize HRP enzymatic reaction. TMB was catalyzed by HRP to produce a blue color product that changed into yellow after adding acidic stop solution. The density of yellow is proportional to the target amount of sample captured in plate. Read the O.D. absorbance at 450nm in a microplate reader, and then the concentration of target can be calculated.

NCBI and Uniprot Product Information

• NCBI GI #: 307574674
• NCBI GeneID: 9217
• NCBI Accession #: NP_001182606.1
• NCBI GenBank Nucleotide #: NM_001195677.1
• UniProt Accession #: O95292; O95293; Q9P0H0; A2A2F2
• Molecular Weight: 11,152 Da
• NCBI Official Full Name: vesicle-associated membrane protein-associated protein B/C isoform 2
• NCBI Official Synonym Full Names: VAMP (vesicle-associated membrane protein)-associated protein B and C
• NCBI Official Symbol: VAPB
• NCBI Official Synonym Symbols: ALS8; VAP-B; VAMP-B
• NCBI Protein Information: vesicle-associated membrane protein-associated protein B/C; VAMP-associated 33 kDa protein
• UniProt Protein Name: Vesicle-associated membrane protein-associated protein B/C
• Protein Family: Virulence-associated protein
• UniProt Gene Name: VAPB
• UniProt Synonym Gene Names: VAMP-B/VAMP-C; VAMP-associated protein B/C; VAP-B/VAP-C
• UniProt Entry Name: VAPB_HUMAN

NCBI Description

The protein encoded by this gene is a type IV membrane protein found in plasma and intracellular vesicle membranes. The encoded protein is found as a homodimer and as a heterodimer with VAPA. This protein also can interact with VAMP1 and VAMP2 and may be involved in vesicle trafficking. [provided by RefSeq, Jul 2008]

Uniprot Description

VAPB: Participates in the endoplasmic reticulum unfolded protein response (UPR) by inducing ERN1/IRE1 activity. Involved in cellular calcium homeostasis regulation. Defects in VAPB are the cause of amyotrophic lateral sclerosis type 8 (ALS8). ALS8 is a familial form of amyotrophic lateral sclerosis, a neurodegenerative disorder affecting upper and lower motor neurons and resulting in fatal paralysis. Sensory abnormalities are absent. Death usually occurs within 2 to 5 years. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of cases leading to familial forms. Defects in VAPB are a cause of spinal muscular atrophy proximal adult autosomal dominant (SMAPAD); also called late-onset spinal muscular atrophy Finkel type. A form of spinal muscular atrophy, a neuromuscular disorder characterized by degeneration of the anterior horn cells of the spinal cord, leading to symmetrical muscle weakness and atrophy. SMAPAD is characterized by proximal muscle weakness that begins in the lower limbs and then progresses to upper limbs, onset in late adulthood (after third decade) and a benign course. Most of the patients remain ambulatory 10 to 40 years after clinical onset. Belongs to the VAMP-associated protein (VAP) (TC 9.B.17) family. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Membrane protein, integral

Chromosomal Location of Human Ortholog: 20q13.33

Cellular Component: Golgi membrane; Golgi apparatus; endoplasmic reticulum membrane; endoplasmic reticulum; integral to membrane

Molecular Function: protein binding; enzyme binding; protein homodimerization activity; FFAT motif binding; protein heterodimerization activity; microtubule binding; beta-tubulin binding

Biological Process: endoplasmic reticulum organization and biogenesis; cellular calcium ion homeostasis; ER to Golgi vesicle-mediated transport; unfolded protein response, activation of signaling protein activity; sphingolipid metabolic process; positive regulation of viral genome replication; sphingolipid biosynthetic process; unfolded protein response; virus-host interaction; negative regulation of viral protein levels in host cell

Disease: Spinal Muscular Atrophy, Late-onset, Finkel Type; Amyotrophic Lateral Sclerosis 8