AICAR
- Known as:
- AICAR
- Catalog number:
- 1687-250
- Product Quantity:
- 250 mg
- Category:
- -
- Supplier:
- Biovis
- Gene target:
- AICAR
Ask about this productRelated genes to: AICAR
- Gene:
- ATIC NIH gene
- Name:
- 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase
- Previous symbol:
- -
- Synonyms:
- PURH, AICARFT, IMPCHASE
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-15
- Date modifiied:
- 2014-11-19
Related products to: AICAR
Related articles to: AICAR
- The study was constructed for investigating the serum expression levels of ATIC with multiple myeloma (MM) patients and its potential clinical value as a biomarker, and analyzing its association with disease stage, treatment response, genetic characteristics and prognosis. - Source: PubMed
Publication date: 2025/08/30
Gu MengyuanZheng YantingWang YifanWang QicaiWu JingXiong ZengyiNong YanyuHuang ChunniLi ZhongqingLuo JunLing ZhianLi Ruolin - Migraine is a neurological disorder affecting approximately 12% of the population, more frequent in women, causing disability. Preventive treatment is recommended to prevent chronification and analgesics' abuse and to improve quality of life, but not all candidates receive it. Common preventive drugs include amitriptyline, flunarizine, propranolol, and topiramate. Their effectiveness and safety have not yet been assessed in our setting. The objective of this study is to evaluate the effectiveness of these drugs in reducing the monthly migraine days (MMD) and to evaluate their safety. - Source: PubMed
Publication date: 2025/08/26
Giner-Soriano MariaMorros RosaMonfà RamonOuchi DanFernández-García SilviaVedia CristinaBonet Monné SaraCalvo Martínez Eva MaríaCopetti Fanlo SilviaMorollón NoemíBelvís Nieto RobertDelgado-Espinoza Claudia ErikaGarcía-Sangenís Ana - Methotrexate, an immunosuppressant and anticancer drug, promotes glucose uptake and lipid oxidation in skeletal muscle via activation of AMP-activated protein kinase (AMPK). Methotrexate promotes AMPK activation by inhibiting 5-aminoimidazole-4-carboxamide ribonucleotide (ZMP) formyltransferase/inosine monophosphate (IMP) cyclohydrolase (ATIC), which converts ZMP, an endogenous purine precursor and an active form of the pharmacological AMPK activator AICAR, to IMP during de novo purine synthesis. In addition to methotrexate, inhibition of purine synthesis underpins the therapeutic effects of a number of commonly used immunosuppressive, anticancer, and antimicrobial drugs, raising the question of whether activation of AMPK in skeletal muscle could be a recurrent feature of these drugs. Using L6 myotubes, we found that AICAR-induced AMPK activation and glucose uptake were enhanced by inhibitors of the conversion of IMP to GMP (mycophenolate mofetil) or of IMP to AMP (alanosine) as well as by indirect inhibitors of human (trimetrexate) and bacterial ATIC (sulfamethoxazole). 6-Mercaptopurine, which inhibits the conversion of IMP to GMP and AMP, activated AMPK, increased glucose uptake, and suppressed insulin signaling, but did not enhance the effect of AICAR. As determined by measuring oxygen consumption rate, none of these agents suppressed mitochondrial function. Overall, our results indicate that IMP metabolism is a gateway for the modulation of AMPK and its metabolic effects in skeletal muscle cells. - Source: PubMed
Dolinar KlemenMiš KatarinaŠopar KatjaŠutar MatejaBožič MetaKolar MaticHropot TimGarcia-Roves Pablo MChibalin Alexander VPirkmajer Sergej - Although anaplastic lymphoma kinase (ALK) gene fusions are increasingly recognized in newly classified pediatric high-grade gliomas, intracranial low-grade tumors harboring ALK rearrangements remain under characterized in the literature. Herein, we present five cases of low-grade intracranial tumors with ALK rearrangements that were diagnosed at a single institution over a continuous 24-month period. Comprehensive clinicopathological evaluation integrating morphological analysis, immunohistochemical profiling, and molecular characterization of fusion partners was performed. Microscopic examination was performed to assess histologic features. A panel of antibodies were used to evaluate protein expression including ALK, desmin, GFAP, Olig2, S100, NeuN, EMA, and CD34. DNA and RNA sequencing was performed, and potential fusion transcripts were analyzed using seed count and structural chromosomal aberrations. All five tumors harbored structural aberrations involving the ALK locus 2p23, and no additional pathogenic mutations, amplifications, deletions, or fusions were identified in all the cases. Among them, two tumors were inflammatory myofibroblastic tumors (IMT) with SQSTM1::ALK, and NPM1::ALK fusion, respectively. One was a tanycytic supratentorial ependymoma (ST-EPN) with HNRNPA1::ALK fusion, and another was ganglioglioma (GG) with PPP1CB::ALK fusion. Interestingly, one case presented as a low-grade myxoid mesenchymal neoplasm with ATIC::ALK rearrangement that did not fit any existing tumor category. All patients underwent complete tumor resection, and were alive with no signs of recurrence during a follow-up period ranging from 1 to 18 months. In summary, ALK fusions may be shared features of a group of low-grade intracranial tumors including IMT, tanycytic ST-EPN, GG, and ALK-rearranged low-grade myxoid mesenchyma neoplasm. Future studies using larger cohorts are warranted to further characterize their clinical and pathological features. - Source: PubMed
Publication date: 2025/08/09
Mu KunZhang YuYang YuyuWang WeiqingMa RanranWang YanzhaoGong Jie - This study aimed to evaluate the associations between genetic polymorphisms within target genes and clinical response to methotrexate (MTX) in Chinese rheumatoid arthritis (RA) patients. - Source: PubMed
Wang MengqiaoWen QinwenYu HangWu XiudiZhi ShuaiCen Han