Cell Signaling Technology

Product Pathways - Neuroscience

ARALAR/AGC1 (D5I6I) Rabbit mAb #64169

No. Size Price
64169S 100 µl ( 10 western blots ) ¥3,100.00 现货查询 购买询价
64169 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Mouse,Rat, Endogenous 75 Rabbit IgG
IP 1:50

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation,

Specificity / Sensitivity

ARALAR/AGC1 (D5I6I) Rabbit mAb recognizes endogenous levels of total ARALAR/AGC1 protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Arg309 of human ARALAR/AGC1 protein.

IP

IP

Immunoprecipitation of ARALAR/AGC1 from mouse brain extracts. Lane 1 is 10% input, lane 2 is Rabbit (DA1E) mAb IgG XP® Isotype Control #3900, and lane 3 is ARALAR/AGC1 (D5I6I) Rabbit mAb (lane 3). Western blot analysis was performed using ARALAR/AGC1 (D5I6I) Rabbit mAb.

Western Blotting

Western Blotting

Western blot analysis of extracts from mouse brain, mouse testis, and rat brain using ARALAR/AGC1 (D5I6I) Rabbit mAb (upper) and β-Actin (D6A8) Rabbit mAb #8457 (lower).

Background

Mitochondrial carriers are integral proteins of the mitochondrial inner membrane that transport metabolites, nucleotides, and co-factors between the cytosol and the mitochondria (1). The calcium-binding mitochondrial carrier protein ARALAR (SLC25A12, AGC1) is an aspartate-glutamate exchange protein responsible for transporting mitochondrial aspartate across the mitochondrial inner membrane in exchange for cytosolic glutamate (2,3). ARALAR and other proteins of the aspartate-glutamate carrier (AGC) group are required for the transfer of mitochondrial aspartate to the cytosol, a key step in urea synthesis (4). Research studies using ARALAR-knockout mice indicate that ARALAR plays an important role in proper CNS myelination. Mice lacking ARALAR suffer from hypomyelination as a result of a lack of oligodendrocyte maturation caused by decreased brain N-acetylaspartate levels (5). Mutation of the corresponding SLC25A12 gene can result in global cerebral hypomyelination and severe psychomotor retardation, caused by deficient ARALAR activity and limited mitochondrial aspartate efflux (6).

  1. Walker, J.E. and Runswick, M.J. (1993) J Bioenerg Biomembr 25, 435-46.
  2. del Arco, A. and Satrústegui, J. (1998) J Biol Chem 273, 23327-34.
  3. Palmieri, L. et al. (2001) EMBO J 20, 5060-9.
  4. Satrústegui, J. et al. (2007) Physiol Rev 87, 29-67.
  5. Ramos, M. et al. (2011) J Neurosci Res 89, 2008-17.
  6. Wibom, R. et al. (2009) N Engl J Med 361, 489-95.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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