IKAROS _ IKZF1
- Known as:
- IKAROS _ IKZF1
- Catalog number:
- Y214398
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- IKAROS _ IKZF1
Related genes to: IKAROS _ IKZF1
- Gene:
- IKZF1 NIH gene
- Name:
- IKAROS family zinc finger 1
- Previous symbol:
- ZNFN1A1
- Synonyms:
- hIk-1, LyF-1, Hs.54452, IKAROS, PPP1R92
- Chromosome:
- 7p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-23
- Date modifiied:
- 2019-04-23
Related products to: IKAROS _ IKZF1
anti-Ikarosanti-IkarosAnti-Ikaros Antibodyanti-Ikaros type: Primary antibodies host: Mouseanti-IKZF1 (Internal)Anti-IKZF1, Goat Polyclonal to IKZF1, Isotype , Host GoatAnti-Mouse Ikaros Purified 100 ugAnti-Mouse Ikaros Purified 25 ugAnti-Mouse IKZF1 (KIAA4227), Rabbit PolyclonalAntibodies: IKAROS _ IKZF1 HOST: Goat Clonality: pAbAntibodies: IKZF1 _ IKAROS HOST: Goat Clonality: pAbBovine IKAROS family zinc finger 3 (Aiolos) (IKZF3) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine IKAROS family zinc finger 5 (Pegasus) (IKZF5) ELISA kit, Species Bovine, Sample Type serum, plasmaChicken DNA-binding protein Ikaros(IKZF1) ELISA kitChicken DNA-binding protein Ikaros(IKZF1) ELISA kit SpeciesChicken Related articles to: IKAROS _ IKZF1
- Butyrate is one of the three main short-chain fatty acids, and it provides energy, controls the state of the intestinal microbiota and mediates the immune response. Sodium butyrate supplementation improves poultry production and changes the intestinal microbiota dynamically. These changes may affect the liver directly and indirectly through pathways in the gut-liver axis, the bidirectional relationship between the liver and intestines. The study analysed gene expression and methylation in the broiler liver after stimulation by sodium butyrate. - Source: PubMed
Publication date: 2026/03/13
Beldowska AleksandraPietrzak ElżbietaDunisławska Aleksandra - CRBN E3 ligase modulators (CELMoDs) exhibit excellent pharmacological activity by degrading cereblon (CRBN) associated multiple substrates and have become an important field for protein degradation drugs development. Previously, we conducted structural modifications on the quinazolinone-based CELMoD CC-122 to obtain derivative 1, which exhibited enhanced degradative activity, but it had issues with metabolic stability. Herein, we designed, synthesized and evaluated a series of novel quinazolinone derivatives, aiming to optimize degradative activity and metabolic stability. After multiple rounds of modification and screening, we obtained compound 26 (NHWL071065), which demonstrated significantly superior lymphoma cell proliferation inhibition and IKZF1/3 degradation activity compared to compound 1, and also showed a significant improvement in the stability of liver microsomes. Compound 26 demonstrates great potential for further research. This study has laid a solid foundation for us to develop novel CELMoDs with potential for becoming drugs. - Source: PubMed
Publication date: 2026/03/31
Chen PengPeng HongkangLiu ChenLi YuxiangYang TongLi MohanHu ChengxuanLi ShaojieDeng ZihaoWang ZhenLiu Linyi - To investigate the clinical characteristics and prognosis of childhood acute lymphoblastic leukemia (ALL) with rearrangement. - Source: PubMed
Tao Ye-QingCui Ding-DingJia Xiao-PeiLian An-NaQi Wen-JingZhu PingWang Chun-MeiSheng Guang-Yao - Acute lymphoblastic leukemia (ALL) management is evolving from a generalized approach toward a precision medicine paradigm driven by molecular heterogeneity. This review highlights how genomic profiling identifies high-risk subtypes, including KMT2A-rearranged, IKZF1-plus BCR::ABL1-positive, BCR::ABL1-like, and TP53-mutant B-cell ALL, which necessitate tailored therapies. We explore novel strategies such as BH3 mimetics, menin inhibitors, pre-T-cell receptor signaling blockade, and targeted immunotherapy, which show promise in relapsed/refractory and high-risk groups. We also address emerging challenges, including therapy-induced phenotypic escape mechanisms such as lineage switch and antigen loss. The future of ALL therapy lies in integrating these biology-driven approaches to improve outcomes across all age groups. - Source: PubMed
Publication date: 2026/03/30
Saygin CanerWitkowski Matthew TCetin SinanAldoss IbrahimLuskin Marlise R - Rapid progress in leukemia management has increased treatment complexity, resulting in clinical scenarios not fully addressed by standard guidelines. To provide expert guidance, the Bridging the Gaps in Hematology Consensus Conference reunited U.S.-based experts in acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and acute lymphoblastic leukemia (ALL) on February 25-26, 2025. Key consensus recommendations were established across AML, MDS, and ALL. For AML, consensus favored CPX-351 for fit patients with secondary or therapy-related AML, without access to clinical trials, and prioritized clinical trial enrollment for other specific molecular subtypes, including those eligible for menin inhibitors. In MDS, consensus supported moving to a harmonized World Health Organization/International Consensus Classification, diagnosing AML based on genetic markers in conjunction with blast counts, and prioritizing stem cell transplant (HSCT) for high-risk patients regardless of response to hypomethylating therapy, particularly for multi-hit TP53-mutated MDS. For ALL, recommendations highlighted avoiding transplant in most Philadelphia chromosome-positive patients achieving minimal residual disease (MRD)-negativity by noting the high relapse risk with certain IKZF1, CDKN2A/B, and PAX5 aberrations, and administering blinatumomab regardless of MRD status in Philadelphia chromosome-positive and -negative ALL. Areas lacking consensus were also identified, highlighting the need for further research. Future directions include refining treatment sequencing, improving outcomes for high-risk subtypes, evaluating the role of HSCT in the era of novel therapies, and standardizing MRD assessment. This consensus report provides valuable expert insights to inform clinical practice and guide future research in leukemia. - Source: PubMed
Publication date: 2026/03/20
Carraway Hetty EDeAngelo Daniel JWang Eunice SKomrokji Rami SPerl Alexander EZeidan AmerBrunner AndrewLai CatherinePark Jae HZeidner Joshua FWeeks LachelleLuskin Marlise RChandhok Namrata SLoghavi Sanam