ZNFN1A2 antibody - C-terminal region (ARP31676_T100)
- Known as:
- ZNFN1A2 (anti-) - C-terminal region (ARP31676_T100)
- Catalog number:
- arp31676_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNFN1A2 antibody - C-terminal region (ARP31676_T100)
Related genes to: ZNFN1A2 antibody - C-terminal region (ARP31676_T100)
- Gene:
- IKZF2 NIH gene
- Name:
- IKAROS family zinc finger 2
- Previous symbol:
- ZNFN1A2
- Synonyms:
- Helios
- Chromosome:
- 2q34
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-23
- Date modifiied:
- 2016-10-05
Related products to: ZNFN1A2 antibody - C-terminal region (ARP31676_T100)
Related articles to: ZNFN1A2 antibody - C-terminal region (ARP31676_T100)
- Immunosuppressive Tregs, regulated by IKZF2, facilitate tumor immune evasion and resistance to immune checkpoint therapies. Targeted IKZF2 degradation represents a promising strategy for the development of innovative cancer immunotherapeutics. Herein, we designed and synthesized a novel series of phthalazinone-based glutarimide derivatives, identifying compound as a potent, highly selective, and rapid-acting IKZF2 molecular glue degrader. Compound induced robust IKZF2 degradation (DC = 1.78 nM and = 93.2%) via a Cullin-CRBN-dependent pathway, while sparing other CRBN neosubstrates and outperforming the benchmark degrader DKY709. Mechanistically, -induced IKZF2 deletion enhanced the proinflammatory IL-2 production and attenuated the immunosuppressive function of Tregs. Oral administration of triggered rapid, profound, and sustained IKZF2 degradation in mice spleen and thymus. As monotherapy, significantly suppressed B16F tumor growth, and combined with anti-PD-1 antibody therapy exhibited marked synergistic effects. Together, our findings demonstrate as a promising IKZF2 degrader for advancing cancer immunotherapy. - Source: PubMed
Publication date: 2026/04/07
Wang YaleiQi ZhenzeSun ShiyangWei TingWei PengliJia ChangkaiCai XuZhao ZhiyuanQiao MinZou YaxinMu ZhihuiLei XiaofangZhang ZiyunWei XinnaQi JiataoCui SihanYang TingtingZhuang XiaomeiXiao JunhaiZheng ZhibingShang HongzhouLi PengyunLi Song - Regeneration and expansion of regulatory T cells (Treg) by low-dose interleukin-2 (IL-2) therapy is considered a potential treatment strategy for a wide range of autoimmune diseases. To provide a pathophysiologically-based rationale for low-dose IL-2 therapy, we investigated whether reversible defects in the Treg-IL-2 axis emerge in inflammatory myopathies. - Source: PubMed
Publication date: 2026/03/25
Ohmes JustusMonne Luisa RComdühr SaraGerlach FynnGrasshoff HannaDübbers AlexanderMüller AntjeScheffold AlexanderRiemekasten GabrielaAkbarzadeh RezaHumrich Jens Y - Small cell lung carcinoma (SCLC) is classically defined by biallelic inactivation of RB1 and TP53. However, a small subset of tumors retains Rb expression and exhibits distinct molecular features. Here, we report two Rb-retained SCLC cases that expand the biological and therapeutic spectrum of this subgroup. Both tumors occurred in middle-aged women, showed small cell morphology with some variant features, and displayed complex copy number alterations. Case 1 harbored a truncal KRAS p.G12C mutation with high-level amplification of chromosome 11q13-q14, including CCND1, and demonstrated a clinical response to sotorasib. Case 2 harbored a TP53 mutation, CDKN2A loss, STK11 inactivation, and a novel IKZF2::ERBB4 fusion. These findings highlight the molecular heterogeneity of Rb-retained SCLC and demonstrate that this subgroup can harbor clinically actionable oncogenic drivers. Accordingly, routine assessment of Rb expression in SCLC, followed by comprehensive molecular profiling of Rb-retained tumors, is warranted to uncover therapeutically relevant targets. - Source: PubMed
Publication date: 2026/03/11
Zacharias MartinJohn NikolausKashofer KarlPopper Helmut - Identifying genetic mechanisms of inborn errors of immunity (IEI) is important for diagnosis and treatment of patients, yet most patients with suspected IEI have negative genetic testing results. Genetic mosaicism is an emerging mechanism of IEI, but it is challenging to identify. - Source: PubMed
Publication date: 2026/02/05
Schmitz Elizabeth GPaul Alexander JGhosh RajarshiSaucier NerminaKolicheski AnaRisma Samuel IMcDaniels Kristen PLiu MichelleLewis Katie Lde Jesus Adriana AAlehashemi SaraFronick Catrina CStein DavidDominguez DanielaHiraki Linda TLee Jessica HNorman StephaniePeng Christine RWard Brant RPettiford Leah HPlatt AnnaLawrence Monica GRocco Joseph MAl-Herz WaleedZerbe Christa SAtkinson T PrescottPeng Xiao PAllenspach Eric JHoytema van Konijnenburg David PPlatt Craig DElkins MeganWalter Jolan EBleesing Jack JKlion AmyRamaswami RamyaUzel GulbuLionakis Michail SDissanayake DilanSu Helen CCortese IreneFuss Ivan JBergerson Jenna R EDropulic LesiaSereti IriniLisco AndreaItan YuvalMilner Joshua DBogunovic DusanGoldbach-Mansky RaphaelaRao V KonetiDelmonte Ottavia MNotarangelo Luigi DKeller Michael DDurkee-Shock JessicaCohen Jeffrey ISimiluk Morgan NHolland Steven MGriffith MalachiGriffith Obi LVogel Tiphanie PCanna ScottFreeman Alexandra FWalkiewicz Magdalena ACooper Megan A - Adoptive cell therapy (ACT) with regulatory T (Treg) cells offers potential for treating immune-mediated diseases. Ensuring the purity and stability of Treg cell products is critical for safe and effective therapies, particularly when targeting specific self-antigens. The purest products are currently obtained using CD4⁺CD25⁺CD127CD45RA⁺ naïve (n)Treg cells. However, these still include cells lacking key transcription factors FOXP3 and Helios, able to produce inflammatory cytokines. Previously, we identified GPA33 as a surface marker for stable FOXP3⁺Helios⁺ human Treg cells and demonstrated that GPA33 nTreg cell populations maintain higher purity during in vitro expansion compared with standard nTreg cells. However, the definition of the GPA33 population among nTreg cells was arbitrary, and cell yields were low. Here, we show methods to unequivocally identify GPA33⁺ cells within the Treg cell fraction and generate Treg cell products that match nTreg cell populations in size and expansion capacity but exhibit superior FOXP3⁺Helios⁺ purity, lack effector cytokine production, and retain full suppressive function. Combining GPA33 with CD226 exclusion eliminates the need for CD127-based gating. Post-expansion, co-expression of GPA33 with TIGIT reliably identifies lineage-stable Treg cells. Thus, GPA33, alone or with CD226/TIGIT, is a robust marker for isolating Treg cells with enhanced therapeutic safety. - Source: PubMed
Morgana FlorenciaSlot EdithAmsen Derk