|Application ||WB, E|
|Other Accession||NP_848590.3, NP_001008949.1|
|Calculated MW||63395 Da|
|Antigen Region||43-71 aa|
|Other Names||Inositol 1, 5-trisphosphate receptor-interacting protein-like 1, ITPRIPL1, KIAA1754L|
|Target/Specificity||This ITPRIPL1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 43-71 amino acids from the N-terminal region of human ITPRIPL1.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||ITPRIPL1 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Cellular Location||Membrane; Single-pass type I membrane protein|
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Provided below are standard protocols that you may find useful for product applications.
ITPRIPL1 (inositol 1,4,5-triphosphate receptor-interacting protein-like 1), also known as KIAA1754L, is a 555 amino acid protein belonging to the ITPRIP family. ITPRIPL1 is a single-pass type I membrane protein expressed as two isoforms produced by alternative splicing events. The gene that encodes ITPRIPL1 maps to human chromosome 2, the second largest human chromosome, consisting of 237 million bases encoding over 1,400 genes and making up approximately 8% of the human genome. A number of genetic diseases are linked to genes on chromosome 2. Harlequin icthyosis, a rare and morbid skin deformity, is associated with mutations in the ABCA12 gene. The lipid metabolic disorder sitosterolemia is associated with ABCG5 and ABCG8. An extremely rare recessive genetic disorder, Alstr?m syndrome is due to mutations in the ALMS1 gene. It has been hypothesized that human chromosome 2 is the result of an ancient fusion of two ancestral chromosome due to its composition of a vestigial second centromere and vestigial telomeres.
Lim, J., et al. Cell 125(4):801-814(2006)
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