RARA Antibody
- Known as:
- RARA Antibody
- Catalog number:
- abx000697
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- RARA Antibody
Related genes to: RARA Antibody
- Gene:
- RARA NIH gene
- Name:
- retinoic acid receptor alpha
- Previous symbol:
- -
- Synonyms:
- RAR, NR1B1
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-06-09
- Date modifiied:
- 2019-04-23
Related products to: RARA Antibody
Related articles to: RARA Antibody
- Not available. - Source: PubMed
Publication date: 2026/08/20
Zhao LuZhu ZhanwangYang BihuiLi LingshuXiao YinChen ZhenzhenLuo JingHuang HuangLi QingzhaoTan KuiYuan ZhaohuiHu GuoyuYang QiuhongShen Chanjuan - Most acute promyelocytic leukemia (APL), driven by the PML::RARA fusion, are now cured with targeted therapies combining all-trans retinoic acid (ATRA) and arsenic trioxide. Some patients treated with earlier ATRA/chemotherapy regimen developed resistance associated with mutations that most often preclude PML::RARA ATRA-binding. Here, we characterized a subset of clustered mutations associated with ATRA-resistance, but not predicted to affect ATRA binding. Most mutants indeed retained full ligand responsiveness, but displayed a basal super-repressive phenotype which did not result from an increased affinity for known corepressors such as NCoR and SMRT. Our findings suggest these mutations are gain-of-function associated with enhanced interactions with unidentified RARA partners with repressive ability. Similar to ATRA-resistant PLZF::RARA variants, these observations stress the role of persistent transcriptional repression of some retinoic acid target genes in acquired ATRA-resistance. - Source: PubMed
Publication date: 2026/08/13
Barbosa Glauce MYuan HaoTambones IzabellaStote Roland HWu Hsin ChiehDe Thé HuguesLe Maire AlbaneGeoffroy Marie-Claude - Aging drives metabolic decline and the accumulation of senescent cells that evade immune clearance. The mechanisms linking host-microbiome co-metabolism to peripheral tissue deterioration remain unclear. We hypothesized that age-dysregulated enterohepatic bile acid (BA) signaling directly promotes systemic aging and immune senescence. - Source: PubMed
Publication date: 2026/07/28
Tan JinzhuoXiong WenyanFeng YingnaLi XingjieJiang HongyuZhang Zongde - Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia characterized by the PML-RARA fusion gene and a high risk of coagulopathy. Type 2 diabetes mellitus (T2DM) is increasingly diagnosed in children and adolescents. To our knowledge, the concomitant diagnosis of these two conditions in the pediatric population has not been previously reported. We report the case of a 10-year-old girl presenting with fatigue, abdominal pain, and fever. Laboratory investigations revealed severe thrombocytopenia, leukocytosis, and 63% circulating blasts on peripheral blood smear. Bone marrow aspiration, immunophenotyping, and molecular analysis confirmed APL through detection of the t(15;17)(q24.1;q21.2) translocation and PML-RARA fusion gene. Based on a white blood cell count of 16.9 × 10⁹/L and a platelet count of 10 × 10⁹/L, the patient was classified as high-risk APL according to the Sanz classification. Severe disseminated intravascular coagulation was present at diagnosis. Concurrent metabolic evaluation demonstrated marked hyperglycemia, elevated HbA1c (8.1%), hyperinsulinemia, atherogenic dyslipidemia, and negative pancreatic autoantibodies, supporting a concomitant diagnosis of T2DM in the setting of overweight status, acanthosis nigricans, and a positive family history. Treatment was initiated according to the AML-MA 2011 induction protocol, comprising cytarabine and daunorubicin combined with all-trans retinoic acid (ATRA), intensive transfusion support, and a basal-bolus insulin regimen. At 18 months of follow-up, the patient remained in complete hematological remission under joint hematological and endocrinological surveillance. This case highlights the importance of considering metabolic disorders in children with hematologic malignancies who present with risk factors for insulin resistance. Emerging evidence suggests potential biological links between metabolic dysregulation and hematological malignancies. Early multidisciplinary management enabled successful control of both conditions and a favorable clinical outcome. - Source: PubMed
Publication date: 2026/06/28
El Hachmi IkramGhanam AyadElouali AzizaSeddik RachidRkain Maria - Lung cancer is the leading cause of cancer-related mortality worldwide, with LUAD being characterized by high incidence and mortality rates. Despite the use of various treatments, including surgery, chemotherapy, immunotherapy, and molecular targeted therapy, the prognosis in LUAD patients remains unfavorable. As a result, the diagnosis and management of LUAD still present major challenges. There is an urgent need to identify novel therapeutic targets. In this study, we analyzed to explore single-cell transcriptomic data (GSE253013 dataset) to investigate epithelial cells heterogeneity in LUAD. Tumor-specific epithelial subpopulations were identified, and the signature genes were evaluated for prognostic, diagnostic potential across several GEO datasets. Functional assays were conducted to validate the role of CRABP2 in lung cancer cells. Xenograft mouse models, rescue experiments and mechanistic analyzes involving ATRA-RAR signaling were further performed to elucidate the molecular mechanism. CRABP2 expression was positively correlated with MDK in LUAD. Functional assays demonstrated that CRABP2 promoted cell proliferation, migration, invasion, and vasculogenic mimicry through activation of the MDK/VEGF/MMP2/9/AKT signaling axis. In vivo xenograft experiments further confirmed that CRABP2 knockdown suppressed tumor growth and angiogenesis. Rescue experiments identified MDK as a critical downstream effector of CRABP2. Mechanistically, CRABP2 enhanced MDK transcription via activation of the ATRA-RAR signaling pathway and increased RARA occupancy at the MDK promoter. Clinically, elevated CRABP2 expression was associated with poor prognosis and showed strong diagnostic performance in LUAD. Collectively, our findings identify CRABP2-ATRA-RAR-MDK signaling axis that drives LUAD progression and angiogenesis. CRABP2 promotes MDK transcription through activation of RAR signaling, thereby enhancing malignant phenotypes and vasculogenic mimicry. These results establish CRABP2 as a promising diagnostic and prognostic biomarker and suggest that targeting the CRABP2-MDK axis may represent a potential therapeutic strategy for LUAD. - Source: PubMed
Publication date: 2026/07/19
Zhang JingshunZhang CuiJiang GuopengLiu XiaLi YifanWang FumanSun XuefeiSun Peidao