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ALS2CR2 Antibody (C-term L289)
Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
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- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | Q9C0K7 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 47026 Da |
| Antigen Region | 274-303 aa |
| Gene ID | 55437 |
|---|---|
| Other Names | STE20-related kinase adapter protein beta, STRAD beta, Amyotrophic lateral sclerosis 2 chromosomal region candidate gene 2 protein, CALS-21, ILP-interacting protein, Pseudokinase ALS2CR2, STRADB, ALS2CR2, ILPIP |
| Target/Specificity | This ALS2CR2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 274-303 amino acids from the C-terminal region of human ALS2CR2. |
| Dilution | WB~~1:1000 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS. |
| 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 | ALS2CR2 Antibody (C-term L289) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | STRADB |
|---|---|
| Synonyms | ALS2CR2, ILPIP |
| Function | Pseudokinase which, in complex with CAB39/MO25 (CAB39/MO25alpha or CAB39L/MO25beta), binds to and activates STK11/LKB1. Adopts a closed conformation typical of active protein kinases and binds STK11/LKB1 as a pseudosubstrate, promoting conformational change of STK11/LKB1 in an active conformation (By similarity). |
| Cellular Location | Nucleus. Cytoplasm |
| Tissue Location | Highly expressed in heart, skeletal muscle, testis, liver and colon. |
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Provided below are standard protocols that you may find useful for product applications.
Background
ALS2CR2 potentiates the antiapoptotic activity of XIAP by enhancing XIAP-mediated activation of JNK1 (MAPK8) and other JNK family members, but not by modulating XIAP-mediated caspase inhibition. Expression of a catalytically inactive TAK1 (MAP3K7) mutant blocks the XIAP/ALS2CR2 activation of JNK1. In vivo coprecipitation experiments show that both ALS2CR2 and XIAP interact with TAK1 and TRAF6. It has been proposed that XIAP-mediated protection from apoptosis utilizes both a JNK1 activation pathway that involves ALS2CR2 and a caspase inhibition pathway that is independent of ALS2CR2.
References
Nishigaki, K., et al., J. Biol. Chem. 278(15):13520-13530 (2003).
Sanna, M.G., et al., J. Biol. Chem. 277(34):30454-30462 (2002).
Hadano, S., et al., Genomics 71(2):200-213 (2001).
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