HIC1 antibody
- Known as:
- HIC1 (anti-)
- Catalog number:
- orb32230
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- HIC1 antibody
Related genes to: HIC1 antibody
- 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
Related articles to: HIC1 antibody
- The myotendinous junction (MTJ) is the critical interface connecting muscle to tendon, enabling force transmission for movement and serving as the primary site of muscle injuries. Despite research into MTJ repair, treatment outcomes are suboptimal, partly due to the absence of a comprehensive synthesis of its structural components, cellular diversity, and developmental mechanisms, which impedes the rational selection of materials, cells, and regulatory factors for effective regeneration. This review synthesizes current knowledge on the cytoskeletal and extracellular matrix (ECM) architecture of the MTJ, the cell types involved in its development and repair, and the key molecular regulators governing its formation. We describe the hierarchical architecture of the MTJ and the key molecular complexes that mediate the mechanical connection between the muscle and the tendon. We also describe the roles of Col22a1-expressing muscle nuclei and various resident stem/progenitor cells in MTJ maintenance and healing. We discuss essential regulatory signaling pathways, including Slit, LRT, and BMP4. Furthermore, we evaluate existing MTJ repair strategies. Based on a review of MTJ development and injury repair, we observe that current treatment approaches largely fail to incorporate key insights from MTJ development, particularly regarding stem/progenitor cells and regulatory signals. Therefore, we propose that tissue engineering techniques, by integrating MTJ-resident stem/progenitor cells such as CD106CD24muscle-tendon progenitors (MTPs) and Hic1Col22a1 progenitors, key MTJ developmental regulatory signals like Slit, Lrt, and BMP4, as well as MTJ decellularized ECM scaffolds or biomimetic 3D-printed scaffolds, will substantially enhance the efficacy of MTJ repair therapies. - Source: PubMed
Publication date: 2026/04/27
Yang KunYin ZiFan Chunmei - Abnormal glucose metabolism often contributes to myofibroblast activation and the pathogenesis of skin fibrotic diseases. All-trans retinoic acid (ATRA), the active component of tretinoin cream, can regulate glucose metabolism and activate myofibroblasts. Importantly, investigating the potential of ATRA to inhibit myofibroblast activation by modulating glucose metabolism could reveal the translational significance of ATRA in attenuating hypertrophic scar (HS) formation. - Source: PubMed
Publication date: 2026/04/27
Li Zi-ChaoZhu Yi-FuSong Ya-JuanTan Zhi-JunLiu BinJiang YanXiao Hou-AnZu Dong-MeiWang TongShi YiJiao YanLi Xue-YongXu Xing-BoShang LeiYu ZhouSong Bao-Qiang - 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
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