HIC1 Antibody (monoclonal) (M02)
- Known as:
- HIC1 Antibody (mab) (M02)
- Catalog number:
- AT2368a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- HIC1 Antibody (monoclonal) (M02)
Related genes to: HIC1 Antibody (monoclonal) (M02)
- Gene:
- EMC10 NIH gene
- Name:
- ER membrane protein complex subunit 10
- Previous symbol:
- C19orf63
- Synonyms:
- INM02, HSS1, HSM1
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2007-07-17
- Date modifiied:
- 2016-12-01
- 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
- Gene:
- MRPL1 NIH gene
- Name:
- mitochondrial ribosomal protein L1
- Previous symbol:
- -
- Synonyms:
- BM022
- Chromosome:
- 4q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-28
- Date modifiied:
- 2015-08-25
- Gene:
- PMS2 NIH gene
- Name:
- PMS1 homolog 2, mismatch repair system component
- Previous symbol:
- PMSL2
- Synonyms:
- H_DJ0042M02.9, HNPCC4, MLH4
- Chromosome:
- 7p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-13
- Date modifiied:
- 2019-04-23
- Gene:
- SESN2 NIH gene
- Name:
- sestrin 2
- Previous symbol:
- -
- Synonyms:
- SES2, DKFZp761M0212, HI95, SEST2
- Chromosome:
- 1p35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-03
- Date modifiied:
- 2016-10-05
Related products to: HIC1 Antibody (monoclonal) (M02)
Related articles to: HIC1 Antibody (monoclonal) (M02)
- Cell migration and strategic positioning within tissues is critical for the rapid mobilization of a T cell response. T cells must remain motile in both lymphoid and nonlymphoid tissues, which vary widely in mechanical properties such as stiffness. Here we showed that activated T cells sensed mechanical cues and responded with changes in cell morphology, nuclear envelope composition and initiation of DNA repair to protect their genomic material from force-mediated damage. Increased mechanical input also drove the transcriptional reprogramming of activated T cells, including changes in many of the core genes shared by tissue-resident memory T cells across diverse tissues, by modulating the expression of the tissue-resident memory T cell-associated transcription factors Klf2, Runx3 and Hic1. Thus, mechanosensing by activated T cells impacted T cell fate, promoting a transcriptional program associated with tissue residency. - Source: PubMed
Publication date: 2026/07/03
Postat JérémyMerino MauricioMingarelli Angela RCerf AyshaBhagrath AanyaPatel DhaneshShen ConnieBrodbeck JohannaTirgar PouriaRogers DakotaBlanc JulesJeyakumar ThiviyaSchneider CaitlinColey ShanaGiannetti NadiaDePauw Taylor ATextor JohannesEhrlicher AllenJameson Stephen CSharif-Naeini RezaSharma AbhinavMandl Judith N - Cardiac hypertrophy plays an important role in organ damage caused by hypertension and may progress into heart failure. This study investigated the function and underlying mechanisms of phosphofurin acidic cluster sorting protein 2 (PACS2) in relation to cardiac hypertrophy. - Source: PubMed
Publication date: 2026/05/14
Shen ZhijieZhang YinzhuangFang Li - 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