ANKHD1
- Known as:
- ANKHD1
- Catalog number:
- 001588A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ANKHD1
Related genes to: ANKHD1
- Gene:
- ANKHD1 NIH gene
- Name:
- ankyrin repeat and KH domain containing 1
- Previous symbol:
- -
- Synonyms:
- MASK, FLJ20288, FLJ11979, FLJ10042, FLJ14127, KIAA1085, MASK1
- Chromosome:
- 5q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-16
- Date modifiied:
- 2015-03-24
Related products to: ANKHD1
Related articles to: ANKHD1
- Cigarette smoking significantly accelerates the initiation and progression of colorectal cancer (CRC), although the precise molecular mechanisms remain incompletely elucidated. Among tobacco-derived carcinogens, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a key one, which has been demonstrated to enhance the malignant progression of CRC. CUT&RUN-seq and mRNA-seq analyses, along with subsequent validation experiments, reveal that NNK upregulates the expression of the acetyltransferase p300. This, in turn, mediates an increase in H3K27ac modification levels at the ANKHD1 promoter, thereby promoting ANKHD1 expression. Furthermore, high expression of ANKHD1 is significantly correlated with poor prognosis in CRC patients. Phenotypic experiments demonstrate that, compared to p300 overexpression alone, combined p300 overexpression with ANKHD1 knockdown partially suppresses the proliferation and metastatic capacity of CRC cells. This suggests that NNK may promote malignant CRC progression by upregulating the p300-ANKHD1 signaling axis. Further mechanistic investigations indicate that the scaffold protein ANKHD1 directly interacts with RBM39 to facilitate the splicing and expression of MKI67 pre-mRNA, thereby driving the malignant progression of NNK-exposed CRC cells. In summary, this study provides novel insights, proposing that targeting the p300-mediated H3K27ac modification pathway to suppress ANKHD1 expression may represent a promising therapeutic strategy and prognostic marker for CRC patients with a history of smoking. - Source: PubMed
Publication date: 2026/04/28
Jiang MinZhao YutingMa QunDing KunHuang YefeiChen Yansu - Identifying patients most likely to benefit from immune checkpoint inhibitors (ICIs) remains a significant challenge in advanced melanoma. We evaluated the association between tumor somatic mutations and clinical outcomes, focusing on relapse-free survival (RFS) and overall survival (OS) in locoregionally advanced melanoma patients treated with neoadjuvant ipilimumab. Tumor specimens and matched peripheral blood samples from 22 patients underwent whole-exome sequencing (WES) to identify non-synonymous somatic mutations. Tumor mutational burden (TMB) was quantified, and specific mutations were analyzed for associations with survival outcomes. The analysis revealed a mutational landscape dominated by single-nucleotide missense mutations with a median TMB of 11.4 mutations/MB. and mutations were detected in 73% of patients and exhibited mutual exclusivity and concurrence patterns ( < 0.05). Positional clustering identified and as key contributors to melanoma (FDR -value < 0.05). Log-rank analysis indicated that mutations in , , , , , , and were associated with shorter survival outcomes (RFS or OS). The associations remained significant in both univariate and multivariable Cox regression models adjusted for TMB. These genes can be broadly grouped into functional categories relevant to tumor progression and immune modulation. In applying multiple testing correction, none maintained statistical significance, indicating that these findings should be interpreted as exploratory and require validation in independent cohorts. This study identified tumor genomic alterations associated with clinical outcomes in melanoma patients treated with neoadjuvant ipilimumab, suggesting their potential role in anti-tumor immunity. These findings warrant further investigation in larger cohorts and across other ICIs in melanoma and other malignancies. - Source: PubMed
Publication date: 2026/03/19
Khaksar Mohammad AliEljilany IslamYassine IbrahimYu XiaoqingTeer Jamie KConejo-Garcia Jose RLyons MaureenLaFramboise WilliamTarhini Ahmad A - RNA modification, which is evolutionarily conserved, is crucial for modulating various biological functions and disease pathogenesis. High resolution transcriptome-wide mapping of RNA modifications has facilitated both data resources and computational prediction of RNA modification. While these prediction algorithms are promising, they are limited in interpretability or generalizability, or the capacity for discovering novel post-transcriptional regulations. Here, we present NetRNApan, a deep learning framework for RNA modification site prediction, motif discovery and trans-regulatory factor identification. Using m5U profiles generated by FICC-seq and miCLIP-seq technologies and single-base resolution m6A sites from multiple experiments as cases, we demonstrated the accuracy of NetRNApan with more efficient and interpretive feature representations. For m5U modification, we uncovered five representative clusters with consensus motifs that may be essential by decoding the informative characteristics detected by NetRNApan. Furthermore, NetRNApan revealed interesting trans-regulatory factors and provided a protein-binding perspective for investigating the function of RNA modifications. Specifically, we discovered 21 potential functional RNA-binding proteins (RBPs) whose binding sites were significantly linked to the extracted top-scoring motifs for m5U modification. Two examples are ANKHD1 and RBM4 with potential regulatory function of m5U modifications. Meanwhile, the analysis of convolution layer parameters within the model offers valuable insights into the regulation of m6A in humans. Collectively, NetRNApan demonstrated high accuracy, interpretability and generalizability for study of RNA modification and mRNA regulation. NetRNApan is freely available at https://github.com/bsml320/NetRNApan. - Source: PubMed
Xu HaodongDeng WankunHu RuifengLiu BinfengZhang WenchaoWang LujuanQi LinRen XiaoleiTu ChaoLi ZhihongZhao Zhongming - A chimeric antigen receptor (CAR) CD30/CD4 T cell lymphoma (TCL) manifested as a single oral ulceration 22 months after treatment with tisagenlecleucel (tisa-cel), an anti-CD19 CAR T cell-based therapy. The TCL showed lentiviral integration in ANKHD1-EIF4EBP3, loss of function of TET2, and NTRK1 copy number gain, suggesting that genetic alterations unrelated to insertional mutagenesis contributed to lymphomagenesis. The patient remains in remission 2 years after radiotherapy. This is the only CARTCL case reported at the Ohio State University James Comprehensive Cancer Center out of 288 patients treated with CAR-T cells. - Source: PubMed
Publication date: 2025/09/02
Bezerra EvandroLupu Ludmilade Lima MarcosPfaller LenaNeal AlisonHajizadeh Nelly RZhao QiuhongBeibel MartinChung CatherineLemmens MyriamSim AustinOertli MevionVoorhees TimothyBohnert RebeccaDenlinger NathanGilbart YoannBontadelli LaraMonovich LauraWillert JenniferStover DanielGao JingboLi LiReinker StefanNaumann UlrikeMenssen Hans DJones DanielLibertini SilvanaBrammer Jonathan E - Using the fly eye as a model system, we previously demonstrated that upregulation of the fly gene protects against FUS- and Tau-induced photoreceptor degeneration. Building upon this finding, we investigated whether the protective role of is conserved in mammals. To this end, we generated a transgenic mouse line carrying Cre-inducible , the human homolog of Utilizing the TauP301S-PS19 mouse model for Tau-related dementia, we found that expressing ANKHD1 driven by CamK2a-Cre reduced hyperphosphorylated human Tau in 6-month-old mice. Additionally, ANKHD1 expression was associated with a trend toward reduced gliosis and preservation of the presynaptic marker Synaptophysin, suggesting a protective role of ANKHD1 against TauP301S-linked neuropathology. At 9 months of age, novel object recognition (NOR) testing revealed cognitive impairment in female, but not male, PS19 mice. Notably, co-expression of ANKHD1 restored cognitive performance in the affected female mice. Together, this study highlights the novel effect of ANKHD1 in counteracting the adverse effects induced by the mutant human Tau protein. This finding underscores ANKHD1's potential as a unique therapeutic target for tauopathies. - Source: PubMed
Publication date: 2025/08/04
Tian XiaolinLe NathanZhao YuhaiAlawamleh DinaSchwartz AndrewMeyer LaurenHelm ElizabethWu Chunlai