HIC1 antibody - N-terminal region (ARP32623_P050)
- Known as:
- HIC1 (anti-) - N-terminal region (ARP32623_P050)
- Catalog number:
- arp32623_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- HIC1 antibody - N-terminal region (ARP32623_P050)
Related genes to: HIC1 antibody - N-terminal region (ARP32623_P050)
- Gene:
- HIC1 NIH gene
- Name:
- HIC ZBTB transcriptional repressor 1
- Previous symbol:
- -
- Synonyms:
- ZBTB29, ZNF901
- Chromosome:
- 17p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-03-19
- Date modifiied:
- 2016-10-03
Related products to: HIC1 antibody - N-terminal region (ARP32623_P050)
Related articles to: HIC1 antibody - N-terminal region (ARP32623_P050)
- DICER1-related tumor predisposition (DRTP), also known as DICER1 syndrome, encompasses a spectrum of malignancies mainly in children and young adults. Most are sarcomas, exhibiting histological and molecular similarities regardless of their anatomical origins, and only express the RNase IIIb domain-defective DICER1. To uncover their cellular origin and developmental hierarchy, we establish a lineage-traceable genetically engineered mouse model with controlled activation of hemizygous Dicer1 RNase IIIb mutation in Hic1 mesenchymal stromal cells. This causes renal tumors closely mirroring the developmental continuum of human DRTP sarcoma histologically and molecularly. Spatial single-cell transcriptomic analysis reveals a Hic1PdgfraDptPi16 fibroblastic progenitor population, corresponding to universal fibroblasts subjacent to transitional epithelium of renal collecting ducts, that can undergo rhabdomyoblastic differentiation or become proliferative sarcomatous cells. Investigation of patient samples identifies analogous cell states and developmental trajectories. This study uncovers a fibroblastic origin for DRTP sarcoma and provides a faithful mouse model for future mechanistic and translational investigation. - Source: PubMed
Publication date: 2026/03/30
Kommoss Felix K FZhang Joyce Yu HanLynch Branden JChen Shary YutingSenz JanineMoscovitz YanaHill Lesley AMa DingScott R WilderBush JonathanChen Kenneth SRoth Andrewvon Deimling AndreasFoulkes William DMorin Gregg BUnderhill T MichaelWang YeminHuntsman David G - Alternative splicing (AS) is a key driver of transcriptomic diversity and plays a pivotal role in epithelial-mesenchymal transition (EMT). During EMT, dynamic splicing changes contribute to cell plasticity and metastasis, yet the upstream regulatory logic remains unclear. Although transcription factors (TFs) are thought to influence AS programs, they typically act through RNA-binding proteins (RBPs), forming a hierarchical TF$\rightarrow $RBP$\rightarrow $AS cascade. Current computational strategies struggle to recover such multi-layered regulation from bulk cross-sectional data, limiting our ability to identify TFs that ultimately control EMT-related AS events. To address this gap, we developed CTAS, a network control theory-based approach to identify key regulatory TFs of AS events during EMT. CTAS integrates pseudotime ordering, trend analysis, sparse directed network inference, and control-theoretic screening into a unified framework. In simulations, CTAS reconstructs EMT trajectories with Spearman's $\rho = 0.99946$ and directed networks with ROC AUC = 89.9%, and remains robust under noise. Applied to a TCGA BRCA cohort, CTAS builds a directed TF$\to $RBP$\to $AS network and identifies HOXA3 (1.00), PRDM8 (0.86), and TWIST2 (0.83) as top TF controllers, alongside significant dynamic shifts in nine AS events detected by Wilcoxon test ($P <.05$). A focused CD44 subnetwork further highlights ZNF521 (0.86) and HIC1 (0.65) as candidate regulators. These findings demonstrate that CTAS transforms cross-sectional data into dynamic regulatory insights and yields experimentally testable TFs that control AS during EMT. - Source: PubMed
Gan YanHe YangsongZhao PuChing Wai-KiQiu Yushan - CD8 T cells differentiate into diverse states that shape immune outcomes in cancer and chronic infection. To define systematically the transcription factors (TFs) driving these states, we built a comprehensive atlas integrating transcriptional and epigenetic data across nine CD8 T cell states and inferred TF activity profiles. Our analysis catalogued TF activity fingerprints, uncovering regulatory mechanisms governing selective cell state differentiation. Leveraging this platform, we focused on two transcriptionally similar but functionally opposing states that are critical in tumour and viral contexts: terminally exhausted T (TEX) cells, which are dysfunctional, and tissue-resident memory T (T) cells, which are protective. Global TF community analysis revealed distinct biological pathways and TF-driven networks underlying protective versus dysfunctional states. Through in vivo CRISPR screening integrated with single-cell RNA sequencing (in vivo Perturb-seq) we delineated several TFs that selectively govern TEX cell differentiation. We also identified HIC1 and GFI1 as shared regulators of TEX and T cell differentiation and KLF6 as a unique regulator of T cells. We discovered new TEX-selective TFs, including ZSCAN20 and JDP2, with no previous known function in T cells. Targeted deletion of these TFs enhanced tumour control and synergized with immune checkpoint blockade but did not interfere with T cell formation. Consistently, their depletion in human T cells reduces the expression of inhibitory receptors and improves effector function. By decoupling exhaustion T-selective from protective T cell programmes, our platform enables more precise engineering of T cell states, accelerating the rational design of more effective cellular immunotherapies. - Source: PubMed
Publication date: 2026/02/04
Chung H KayLiu CongBattu AnamikaJambor Alexander NPratt Brandon MXie FucongRiesenberg Brian PCasillas EduardoSun MingLandoni ElisaLi YanpeiYe QidangJoo DanielGreen JarredSyed ZaidBrown Nolan JSmith MatthewMa ShixinTan ShirongChick BrentTripple VictoriaWang Z AudreyWang JunMcdonald BryanHe PeixiangYang QiyuanChen TimothyVaranasi Siva KarthikLaPorta Michael AMann Thomas HChen DanHoffmann FilipeHo JosephineModliszewski JenniferWilliams AprilLiu YushaWang ZhenLiu JieyuanGao YimingHu ZhitingCho Ukrae HLiu LongweiWang YingxiaoHargreaves Diana CDotti GianpietroSavoldo BarbaraThaxton Jessica EMilner J JustinKaech Susan MWang Wei - Pulmonary interstitial macrophages can be divided into 2 distinct subsets with different origins: resident macrophages (resMФs) and recruited macrophages (recMФs). However, their specific roles in pulmonary arterial hypertension remain unclear. - Source: PubMed
Publication date: 2025/12/31
Guo ShuminPan TingYan XiaojieCheng YuanyuanDu RongluLiu QianHuang YongleZhuo YujuanZhao YanTian DanyangShi XinxinQiang TitiCao XinTang XiaoqiangKorinek VladimirHuang DandanZhou BinWang Jiong-WeiDong ChengQi YongShen YujunYu Ying - Synovial sarcoma (SyS) is an aggressive soft-tissue malignancy that is characterised by a pathognomonic t(X;18)(p11.2;q11.2) translocation, which produces the fusion oncogene named SS18::SSX. Despite recent advancements in our understanding of synovial sarcoma biology, the cell-of-origin remains undefined. A mesenchymal stromal cell (MSC) specific CreERT2 line was employed to express SS18::SSX in fibroblasts and related cell types, resulting in 100% penetrant synovial sarcoma development in mice, with a median latency period of 16.2 ± 2.8 weeks. Murine tumours exhibited high concordance with human synovial sarcoma subtypes at the histological and molecular levels. Genetic refinement of the cell-of-origin revealed that synovial sarcomas derive from a rare Hic1 Pdgfra Lgr5 fibroblastic population. Furthermore, comparative transcriptomic analysis revealed the acquisition of a transformed phenotype initiated by the loss of a mature fibroblastic profile and subsequent unmasking of an epigenetically embedded embryonic MSC program. Adult and embryonic MSCs exhibited overlapping H2AK119ub and H3K4me3/H3K27me3 (bivalent) histone marks, while SS18::SSX-mediated transformation culminated in the widespread loss of H3K27me3 at these genes and their consequent transcription. Collectively, these studies define a rare MSC context, conducive for SS18::SSX-mediated transformation, and demonstrate that SyS tumorigenesis involves the induction and maintenance of an embryonic-like MSC phenotype. - Source: PubMed
Publication date: 2025/12/02
Hill Lesley AScott R WilderMartin Lauren AArostegui MartinDavenport GeorgeVemon MarcosHofvander JakobWang Xue QiLi JinxiuNielsen Torsten OJones Kevin BHirst MartinUnderhill T Michael