Polyclonal Rabbit IKZF2 Antibody
- Known as:
- Polyclonal Rabbit IKZF2 Antibody
- Catalog number:
- KA1758
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit IKZF2 Antibody
Ask about this productRelated genes to: Polyclonal Rabbit IKZF2 Antibody
- 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: Polyclonal Rabbit IKZF2 Antibody
Related articles to: Polyclonal Rabbit IKZF2 Antibody
- Cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) are the primary histological subtypes of cervical cancer. Although the AGPAT family of enzymes is implicated in various cancer types, the specific roles of its members in cervical cancer remain unclear. In the present study, we investigated the value of AGPAT1-5 as potential biomarkers and therapeutic targets in cervical cancer by assessing their impact on disease development and outcomes. AGPAT gene expression data and clinical information from 306 patients with CESC and three control subjects were collected from The Cancer Genome Atlas. Given the limited number of normal cervical samples in TCGA (n = 3), we utilized the GEPIA database to integrate GTEx normal cervical samples (n = 10) as controls for differential expression analysis. These data were analyzed for differential gene expression, gene-gene and protein-protein interactions, prognostic and diagnostic value, clinical correlations, functional enrichment, and various tumor-infiltrating immune cell types. Validation was performed using two independent Gene Expression Omnibus (GEO) datasets (GSE6791 and GSE63514). The study revealed that AGPAT4 mRNA expression was significantly downregulated in cervical cancer tissues compared to normal tissues in the GEPIA analysis, while AGPAT1, AGPAT2, AGPAT3, and AGPAT5 showed no significant differences. Validation in GEO datasets demonstrated that AGPAT1, AGPAT2, and AGPAT3 were consistently downregulated in tumor tissues, whereas AGPAT5 was upregulated, and AGPAT4 showed no significant change. High levels of AGPAT3 and AGPAT4 expression, in particular, were associated with a worse prognosis in CESC patients. Immune infiltration analysis restricted to CESC samples revealed that AGPAT3 expression was significantly correlated with multiple immune cell types, including positive correlations with Macrophages M1, T cells CD4 memory resting, and Monocytes. Furthermore, guided by functional enrichment analysis implicating immune-related pathways, we examined the correlation between AGPAT3 expression and key T cell regulatory molecules, including FOXP3, IL2RA, IKZF2, and CCR8, revealing significant positive associations. In vitro assays demonstrated that knocking out AGPAT3 expression significantly decreased the proliferation and migration of HeLa and C-33 A cervical cancer cell line. These results suggest that AGPAT3 could be a valuable biomarker and a promising therapeutic target in cervical cancer. - Source: PubMed
Publication date: 2026/06/09
Gui NannanPan HanyiLu WeijuanPan GuiqiongZhou XiaoyuChen YuzhenJin MingyangYang ChangyongDong MingyouLiang Yuexiu - Early life is essential for establishing memory T cells, which rapidly populate mucosal sites during infancy, although these nascent memory T cells are less protective than their adult counterparts. Here we used single-cell RNA sequencing of resting and CD3+CD28 antibody-stimulated T cells from lymphoid and mucosal tissues of infant (2-9 months) and adult (40-63 years) organ donors to investigate age-dependent mechanisms for functional regulation of human memory T cells. Infant CCL5 effector memory T cells exhibited reduced effector function compared to adults. Transcription factor network analysis identified HELIOS and KLF6 as regulators of memory T cell states in infant and adult tissues, respectively. Using single-nucleus RNA sequencing, assay for transposase-accessible chromatin sequencing and CRISPR-Cas9 knockout, we defined HELIOS (IKZF2) as a critical regulator of the infant-specific transcriptional program in CCL5 effector memory T cells and restricted effector function in SELLCCR7 naive and/or central memory T cells. Our findings reveal key mechanisms controlling T cell functional states in early life. - Source: PubMed
Publication date: 2026/06/02
Szabo Peter ALevitin Hanna MNargund SiddhiConnors Thomas JChen DavidJin JennyThapa PuspaGuyer RebeccaCaron Daniel PGray Joshua IMatsumoto ReiKubota MasaruBrusko MaiganBrusko Todd MFarber Donna LSims Peter A - Parkinson's disease (PD) is associated with systemic molecular alterations that extend beyond the central nervous system, including changes in peripheral blood transcriptomic profiles. While prior studies have focused predominantly on coding-gene expression, the longitudinal behavior of the peripheral blood repeatome following clinical diagnosis remains poorly characterized. Here, we investigated temporal remodeling of repetitive-element transcription over 36 months post-diagnosis by integrating repeat subfamily- and locus-specific analyses. - Source: PubMed
Publication date: 2026/05/18
Kulski Jerzy KKoks Sulev - IKAROS, HELIOS, and AIOLOS are transcription factors predominantly expressed in hematopoietic cells, where they form heteromeric and homodimeric complexes and facilitate transcriptional regulation. IKZF proteins also associate with non-IKZF family proteins, which vary between different immune cell subtypes and their differentiation stages. Heterozygous germline loss-of-function variants in , , and cause IKAROS, HELIOS, and AIOLOS deficiencies, respectively, leading to inborn errors of immunity (IEI). Heterozygous gain-of-function (GOF) variants in result in IKAROS-GOF disease, characterized by autoimmune and allergic manifestations, whereas dominant-negative IKAROS and AIOLOS variants are associated with combined immunodeficiency. Importantly, patients with IKZF-associated IEI exhibit varying degrees of immunodeficiency, immune dysregulation, and occasional malignancies, and so, disease manifestations differ significantly among the variant types. Therefore, each variant often causes phenotypic heterogeneity, which possibly stems from diverse protein complexes formed by IKZF proteins. Besides immunoglobulin supplementation for patients with B cell defects and hematopoietic cell transplantation for severe cases, molecularly targeted therapies have been investigated for treating IKAROS-GOF disease. - Source: PubMed
Publication date: 2025/07/18
Yamashita MotoiMorio Tomohiro - Recent studies have advanced understanding of chromosomal organization and its role in gene regulation, yet most analyses focus on short-range interactions (<2 Mb), limiting insight into broader architecture. The relationships between topologically associating domains (TADs), sub-TAD loops, cross-TAD interactions, and chromosomal compartmentalization remain poorly understood. Here, using high-resolution Hi-C analysis, we identify extensive multi-megabase and interchromosomal interactions (metaloops) in T lymphocytes that organize into meta-TAD associations (metadomains). These metaloops connect distal promoters and regulatory elements of genes functionally important in T cells, including Ctla4, Ikzf2, Il2ra, Ets1, and Foxo1. Reanalysis of mouse and human datasets confirms their reproducibility and dependence on superenhancers. Genome-wide clustering reveals three distinct interchromosomal hubs, including a superenhancer-enriched hub linked to T cell-specific gene activation. Integrative analysis of regulatory genomics data identifies factors associated with short- versus long-range interactions. This study introduces a broadly applicable computational framework and reveals features of T cell genome organization. - Source: PubMed
Publication date: 2026/05/08
Dolsten GabrielWang Zhong-MinHuang XiaoSong SusieWilson Michael JBing Xin YangKe WenfanCafiero Thomas RNelson Amy NFernando SebastianPloss AlexanderSchedl PaulLevine Michael SViny Aaron DRudensky Alexander YPritykin Yuri