VAPB / VAMP-associated B/C Recombinant Protein | VAPB recombinant protein

Recombinant Human VAPB / VAMP-associated protein B/C Protein (His tag)

Cat. Num. AAA2546100

• Gene Names: VAPB; ALS8; VAP-B; VAMP-B
• Purity: > 97 % as determined by SDS-PAGE
• Synonyms: VAPB / VAMP-associated B/C; Recombinant Human VAPB / VAMP-associated protein B/C Protein (His tag); RP5-1018E9.1; ALS8; VAMP-B; VAP-B; VAPB recombinant protein

• Host: E Coli
• Purity/Purification: > 97 % as determined by SDS-PAGE
• Form/Format: Lyophilized from sterile PBS, pH 8.0
• Sequence Length: 99

• Application Notes: The recombinant human VAPB consisting of 142 amino acids and has a calculated molecular mass of 16.3 kDa. It migrates as an approximately 18 kDa band in SDS-PAGE under reducing conditions.
• Predicted N Terminal: Met
• Preparation and Storage: Samples are stable for up to twelve months from date of receipt at -70 degree C

SDS-PAGE

Related Product Information for VAPB recombinant protein

Background: Vesicle-associated membrane protein-associated protein B / C, also known as VAMP-B/VAMP-C, VAMP-associated protein B/C, VAP-B/VAP-C and VAPB, is a single-pass type IV membrane protein which belongs to the VAMP-associated protein (VAP) family. VAPB contains one MSP domain. VAPB may play a role in vesicle trafficking. VAPB forms a heterodimer with VAPA. VAPB interacts with VAMP1 and VAMP2. Defects in VAPB are the cause of amyotrophic lateral sclerosis type 8 (ALS8) which is a familial form of amyotrophic lateral sclerosis, a neurodegenerative disorder affecting upper and lower motor neurons and resulting in fatal paralysis. Defects in VAPB are also a cause of spinal muscular atrophy autosomal dominant Finkel type (SMAF) which is characterized by proximal muscle weakness that begins in the lower limbs and then progresses to upper limbs.

Description: A DNA sequence encoding the human VAPB (O95292-1) N-terminal fragment (Met 1-Pro 132) was fused with a polyhistidine tag at the C-terminus.

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 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
• 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

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: 20q13.32

Cellular Component: cell-cell adherens junction; cytoplasm; endoplasmic reticulum; endoplasmic reticulum membrane; Golgi apparatus

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

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

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