ACRBP
- Known as:
- ACRBP
- Catalog number:
- 001038A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACRBP
Related genes to: ACRBP
- Gene:
- ACRBP NIH gene
- Name:
- acrosin binding protein
- Previous symbol:
- -
- Synonyms:
- SP32, OY-TES-1, CT23
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-19
- Date modifiied:
- 2009-03-12
Related products to: ACRBP
Related articles to: ACRBP
- BACKGROUND: The testis exhibits the highest tissue-specific gene expression of all organs, including both coding and non-coding genes. Our previous study reported that Teshl, a testis-specific long noncoding RNA, associates with heat shock factor 2 (HSF2), a transcription factor, to regulate Y chromosome gene expression and sperm fertility. RESULTS: We conducted an in-depth analysis of the function and molecular mechanisms of Teshl using Teshl-knockout (KO) mice. Remarkably, the absence of Teshl caused abnormal acrosome biogenesis during spermiogenesis, resulting in malformed and disorganized acrosomes and abnormal sperm head morphology. Teshl-KO sperm also exhibited altered acrosome reaction and reduced motility. A thorough examination of all available relevant datasets identified three Teshl-related proteins associated with acrosome structure and function: actin related protein T1 (ACTRT1), acrosin binding protein (ACRBP) and dickkopf-like acrosomal protein 1 (DKKL1). Our findings suggest that these proteins are directly or indirectly regulated by Teshl-HSF2 through transcriptional or protein-interaction mechanisms. CONCLUSIONS: The present findings significantly expand our understanding of the important roles of Teshl, a pioneering testis-specific lncRNA, by elucidating its acrosomal function and mechanism in male reproduction. - Source: PubMed
Publication date: 2026/03/30
Hong Seung PyoHong Seong HyeonHan GwidongLee Seung JaeOh YoungsooCho Chunghee - Acute myeloid leukemia (AML) remains a challenging hematologic malignancy with poor survival rates, underscoring the need for precise prognostic biomarkers and therapeutic strategies. Cancer-testis antigens (CTAs), with tumor-restricted expression and immunogenicity, have not been systematically explored for prognosis prediction in AML. Here, we developed a novel CTA-based prognostic signature to predict survival and immunotherapy response in AML patients. Utilizing RNA-seq and clinical data from the TCGA-Acute Myeloid Leukemia cohort (n = 126, training set) and the GSE71014 dataset (n = 104, validation set), we identified 21 prognosis-associated CTAs via univariate Cox regression. Least absolute shrinkage and selection operator and multivariate Cox regression refined the model to 5 key genes: ACRBP, IGF2BP3, SPAG1, TEX101, and KDM5B. The CTA score, calculated from gene expression and regression coefficients, stratified patients into high- and low-risk groups with distinct overall survival (P < .001). The model exhibited robust predictive accuracy, with time-dependent area under the curve values of 0.863 (TCGA-Acute Myeloid Leukemia training set) and 0.723 (GSE71014 validation cohort) for 5-year overall survival. High CTA scores correlated with adverse prognosis, elevated monocytes and M0 macrophages infiltration, and enhanced immunotherapy responsiveness. Functional enrichment analysis revealed dysregulation in several key AML-related pathways, including leukocyte migration, PI3K-Akt signaling, and cytokine pathways. A nomogram integrating CTA score and age further improved prognostic precision (concordance index = 0.77). Drug sensitivity profiling highlighted differential therapeutic vulnerabilities between risk groups. This study established and validated a novel CTA-based prognostic tool for prognostic stratification and personalized treatment guidance in AML, bridging molecular insights with clinical applications. - Source: PubMed
Alip MihribangvlAiniwaer DilimuretiChang HanwenYuan LifengAimaieryili AbudukadierAi WuWang XuejunTuerxun MairanmunishaMusa YaermaimaitiYusuying NuermaimatiMamatkerim NurnisagulTursun Abudukadir - While our prior study identified the HLA-A *0201-restricted ACRBP epitope peptide and demonstrated its capacity to generate cytotoxic T lymphocytes (CTLs) in vitro, the clinical relevance of the peptide-induced T cell reactivity in ovarian cancer (OC) patients and the in vivo anti-tumor efficacy of these CTLs remain unexplored. In this study, dendritic cells were sensitized with ACRBP peptide (ALLVLCYSI) and co-cultured with autologous CD8T cells to induce the production of specific cytotoxic T lymphocytes (Pep-CTLs). The anti-tumor effects of Pep-CTLs were evaluated in SCID mice bearing human ovarian cancer (OC) OVCAR-3 cells. Concurrently, we co-cultured ALLVLCYSI peptide with peripheral blood mononuclear cells (PBMCs) from OC patients (HLA-A2, ACRBP) and assessed the number of specific T cells using ELISPOT assays. The immunological impact of the ACRBP peptide against human OC was validated through both in vitro and in vivo experiments. These findings establish a preclinical foundationfor developing ACRBP peptide-based vaccines in OC immunotherapy. To further elucidate ACRBP's role in OC treatment, the study analyzed single-cell RNA sequencing data from 8 OC patients and bulk RNA sequencing data from the Cancer Genome Atlas Project (TCGA) comprising 308 ovarian cancer cases. This analysis aimed to explore the heterogeneity among ACRBP-expressing tumor cell populations and to investigate the correlation between ACRBP expression and immune molecule expression (including MHC and chemokines) alongside chemotherapy response. These insights furnish a theoretical framework supporting the future application of ACRBP in tumor immunotherapy and strategies to prevent immune escape. - Source: PubMed
Publication date: 2025/10/16
Zeng XiaLin Li-NaLi XiaoquanNong Wei-XiaLi FengLan LiWang PingYe AiZhang Qing-MeiLuo BinGe Ying-YingXie Xiao-Xun - Cancer treatments can lead to infertility, particularly in prepubertal boys who cannot preserve sperm before therapy. In vitro spermatogenesis offers a promising strategy for fertility preservation in this population by enabling the development of sperm from immature testicular tissue under controlled conditions. This study investigates the effects of a novel culture medium containing plasma rich in growth factors (PRGF) and knockout serum replacement (KSR) on in vitro spermatogenesis. Testicular tissues from five-day-old male NMRI mice were cultured in either a medium containing 5% KSR + 5% PRGF or a control medium containing 10% KSR for 42 days. Histological analysis revealed significant degeneration of peripheral seminiferous tubules in the 5% KSR + 5% PRGF group compared to the control. Gene expression analysis showed reduced levels of spermatogenesis markers (Plzf, Tekt1, Tnp1) and the proliferation marker Ki67, alongside elevated expression of the pro-apoptotic marker Bax. Immunofluorescence confirmed fewer spermatogonial stem cells (PLZF), spermatocytes (SYCP3), and proliferating cells (Ki67), with complete absence of post-meiotic marker ACRBP in the 5% KSR + 5% PRGF group. Additionally, higher Bax and lower Bcl-2 fluorescence intensities were observed in this group. These findings indicate that a medium supplemented with 5% KSR and 5% PRGF is ineffective for supporting complete in vitro spermatogenesis and may promote apoptosis. Importantly, these results provide insights into culture system design for future applications in fertility preservation strategies for prepubertal cancer patients at risk of gonadotoxicity. - Source: PubMed
Publication date: 2025/08/26
Moradian Seyyed AmirKhaledi SajedAmirkhani ZahraMovahedin Mansoureh - Culture medium enriched with Knockout serum replacement (KSR) can produce in vitro mouse sperm, but it is inefficient, strain-specific and contains bovine products, which limits its use in the human clinic. The study aimed to optimize the culture medium for testicular tissue by using plasma rich in growth factors (PRGF) as a serum supplement, addressing the limitations of KSR. - Source: PubMed
Publication date: 2025/01/23
Moradian Seyyed AmirMovahedin Mansoureh