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ATIC (F6Z3O) Rabbit Monoclonal Antibody #66095

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  • WB
  • IP

    Product Specifications

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 65
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    ATIC (F6Z3O) Rabbit Monoclonal Antibody recognizes endogenous levels of total ATIC protein.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro212 of human ATIC protein.

    Background

    5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/inosine monophosphate cyclohydrolase (ATIC) is a bifunctional enzyme, catalyzing the last two steps of de novo purine synthesis (DNPS), converting 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) to inosine monophosphate (IMP). Proliferating cells require enhanced nucleotide synthesis, leading to upregulation of genes associated with DNPS and purine salvage pathways. Altered purine metabolism is linked to increased cell proliferation and cancer development and progression. Enhanced ATIC expression is observed in a variety of cancers and is associated with poor prognosis, promoting cell growth, migration, and resistance to some therapeutic interventions (1-4). Altered purine metabolism also correlates with the progression of Parkinson’s disease (PD). LRRK2 mutations are the most common genetic cause of PD. Research suggests that ATIC and its substrate AICAR may regulate LRRK2 expression levels and toxicity (5). The LRRK2 G2019S mutation, which increases kinase activity, is the most prevalent mutation among those with LRRK2-associated PD. Notably, ATIC was observed to be the most downregulated protein in a cohort of LRRK2 G2019S carriers. These findings suggest that ATIC may be a viable target for therapeutic intervention in PD (6).

    Alternate Names

    5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase; 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase; 5-aminoimidazole-4-carboxamide-1-beta-D-ribonucleotide transformylase/inosinicase; AICAR; AICAR formyltransferase; AICAR formyltransferase/IMP cyclohydrolase bifunctional enzyme; AICAR transformylase; AICAR transformylase/inosine monophosphate cyclohydrolase; AICARFT; AICARFT/IMPCHASE; ATIC; Bifunctional purine biosynthesis protein ATIC; Bifunctional purine biosynthesis protein ATIC, N-terminally processed; Bifunctional purine biosynthesis protein PURH; epididymis secretory sperm binding protein Li 70p; FLJ93545; HEL-S-70p; IMP cyclohydrolase; IMP synthase; IMPCHASE; Inosine 5'-monophosphate cyclohydrolase; Inosinicase; Phosphoribosylaminoimidazolecarboxamide formyltransferase; phosphoribosylaminoimidazolecarboxamide formyltransferase/IMP cyclohydrolase; PUR9; PURH

    For Research Use Only. Not for Use in Diagnostic Procedures.
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