RARA antibody - middle region (P100861_P050)
- Known as:
- RARA (anti-) - middle region (P100861_P050)
- Catalog number:
- p100861_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RARA antibody - middle region (P100861_P050)
Ask about this productRelated genes to: RARA antibody - middle region (P100861_P050)
- 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 - middle region (P100861_P050)
Related articles to: RARA antibody - middle region (P100861_P050)
- Not available. - Source: PubMed
Publication date: 2026/04/23
Yin XiaomeiLi NaCheng ZhanruiAi JiaLiang HongSun ShuZhu Hong-Hu - To observe the incidence of Meniere's disease (MD) and MD-related symptoms (i.e., aural fullness, tinnitus, hearing loss, and vertigo) between (a) non-migraine and migraine patients and (b) migraine untreated and migraine treated patients within the TriNetX database. - Source: PubMed
Publication date: 2026/04/21
Bhatt KhushiRen YueqiChan CharlotteRara MarianneDjalilian Hamid RAbouzari Mehdi - Classical acute promyelocytic leukemia (APL) is defined by the presence of the fusion; however, a subset of acute myeloid leukemia (AML) cases presents with morphological and clinical features highly suggestive of APL despite lacking this canonical rearrangement, creating diagnostic and therapeutic dilemmas. We report a 27-year-old woman initially diagnosed with AML characterized by myeloid sarcoma and a predominance of promyelocytes (44%) in the bone marrow. Fluorescence in situ hybridization and RNA sequencing failed to detect , while targeted sequencing revealed mutations in and . Although complete remission was achieved after induction therapy, the response to IA and subsequent CHA chemotherapy regimens was suboptimal. Two years later, the patient relapsed with severe coagulopathy and a marked increase in promyelocytes (71%). Comprehensive genomic re-evaluation at relapse identified a novel fusion and a rare mutation. Notably, transcriptomic analysis demonstrated marked overexpression of and . Based on these molecular findings, treatment with all-trans retinoic acid combined with intermediate-dose cytarabine was initiated, leading to rapid clinical improvement and achievement of complete remission. This case describes a rare AML entity that closely recapitulates the clinical and molecular features of APL in the absence of and suggests that activation of retinoic acid–responsive pathways, potentially mediated by RARA/RXRA overexpression and novel gene fusions, can occur independently of the canonical rearrangement, with important therapeutic implications. - Source: PubMed
Publication date: 2026/04/18
Ma LinaWu Min - Anorectal malformation (ARM) is the most common congenital digestive tract anomaly in newborns, and children with ARM often have varying degrees of underdevelopment of the pelvic floor muscles (PFMs). To explore the effects of Rarα (NR1B1) and Pitx2 on the development of rat PFMs, we constructed a rat ARM animal model using all-trans retinoic acid (ATRA), and verified the expression of Rarα and Pitx2 in the PFMs of fetal rats. Additionally, we used rat myoblasts (L6 cells) to investigate the regulatory roles of Rarα and Pitx2 in skeletal muscle myoblast differentiation and their interactions. The results indicated a significant decrease in the expression of Rarα and Pitx2 in the PFMs of fetal rats with ARM. ATRA can also decrease the expression of Rarα and Pitx2 in the L6 cells, while affecting the differentiation and fusion of L6 cells. Knocking down Rarα in L6 cells reduced the expression of Pitx2, Myod1, Mymk, and decreased myogenic activity in L6 cells. When Rarα is activated, the decreased expression of Pitx2, Myod1, and Mymk and myogenic differentiation can be restored to different extents. At the same time, increasing or inhibiting the expression of Pitx2 can counteract the effects of knocking down Rarα and activating Rarα respectively. These results indicate that Pitx2 may be downstream of the transcription factor Rarα, mediating the effects of ATRA on the development of fetal rat PFMs. - Source: PubMed
Publication date: 2026/04/17
Zhao HanbinCao JianMu HuaqiBi YangGuo ZhenhuaShi YuanWang Yi - Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia characterized by the fusion gene and frequent coagulopathy. All-trans retinoic acid (ATRA) plus arsenic trioxide (ATO)-based regimens achieve excellent complete remission rates exceeding 95% with durable molecular responses. However, treatment-related and disease-related complications may occur during therapy. We report a case of a 57-year-old man with APL complicated by bone marrow necrosis, pulmonary complications, and posterior reversible encephalopathy syndrome. Multidisciplinary supportive care with continuation of ATRA-ATO therapy resulted in complete hematologic and molecular remission. This case highlights the importance of recognizing and managing complex complications in APL while maintaining curative therapy. - Source: PubMed
Publication date: 2026/03/10
Venou Theodora MMainou MariaVoura KonstantinaMbonde Mouangue Ester SFlaris NicolaosVlachaki Efthymia