Ask about this productRelated genes to: PRSS21 Blocking Peptide
- Gene:
- PRSS21 NIH gene
- Name:
- serine protease 21
- Previous symbol:
- -
- Synonyms:
- ESP-1, TEST1
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-17
- Date modifiied:
- 2018-01-19
Related products to: PRSS21 Blocking Peptide
Related articles to: PRSS21 Blocking Peptide
- Testis Germ Cell Tumor (TGCT) is a most common type of testicular malignancy (95%), manifesting mostly in adult men. In recent studies, TGCT have been characterized by aneuploidy, less alteration in genome and low levels of methylation, apart from pathological characterization. Expression of Cancer- Testis (CT) genes in TGCT have also been observed in tumors arising from non-germ cells. Datasets from different online tools showed that expression of FKBP4 have significant difference in TGCT as compared to the normal testis tissues. In addition, FKBP4 showed increased expression with successive stages of TGCT. The FKBP4 showed positive correlation with SALL4, NANOG, SOX2, OCT4, PRSS21 while negative correlation with MGMT, RASSF1, SOX17 and KIT. Analysis showed the increased hazard ratio (HR) is case of overall survival (OS) as compared to the disease-free survival (DFS) in TGCT patient. Furthermore, gene ontology enrichment analysis was performed with upregulated genes in TGCT using DAVID database. FKBP4 belongs to families of peptidyl proline cis-trans isomerase (PPIase), which catalyses the cis-trans isomerization in peptide bonds which comes before proline. PPIases are engaged in numerous cellular processes, and when these processes go awry, can cause both neoplastic and degenerative disorders. To decipher the pathway regulating the proliferation of TGCT, FKBP4 interaction analysis was conducted using STRING, which shows the interaction with known biomarkers of TGCT. All this dataset of expression profile, correlation, and interaction analysis represents FKBP4 might act as a key player to differentiate subtype of Testis Germ Cell Tumor (TGCT). - Source: PubMed
Publication date: 2026/03/17
Sahni DeepakKumar BhupendraPorwal SaumyaArya Ashutosh KumarAkhtar Md SohailBharati Akhilendra Pratap - This study aimed to investigate differentially expressed mRNA transcripts between patients with heart failure with preserved ejection fraction (HFpEF) exhibiting normal versus elevated B-type natriuretic peptide (BNP) levels, thereby seeking novel early diagnostic molecular biomarkers and therapeutic targets to facilitate precision medicine in heart failure management.First, using mRNA transcriptomics, we analyzed 10 patients with HFpEF and normal BNP levels, 10 patients with HFpEF and elevated BNP levels, and 10 healthy controls. Compared with the BNP elevated group, the BNP normal group exhibited upregulated WEE1, GATA3, MLC1, SH2D1B, NLRP2, and SLC12A1, as well as downregulated ST3GAL6 and NUDT16. Relative to controls, HFpEF-N demonstrated 147 upregulated (e.g., BMP2, GPR84, and IL1B) and 24 downregulated (e.g., HIST1H1B/D and PRSS21) mRNAs. Second, the differentially expressed genes in the BNP normal group were significantly enriched in pathways including mitotic nuclear division (GO:0140014), regulation of hormone metabolic processes (GO:0032350), and regulation of mitotic nuclear division (GO:0007088). In addition, key pathways including IL-17 (hsa04657) and chemokine signaling (hsa04062) were upregulated. Finally, in an additional cohort (60 HFpEF with normal BNP versus 61 HFpEF with elevated BNP), three upregulated mRNAs were validated: GATA3, IFNG, and GPR84. IFNG and GATA3 were significantly upregulated in the BNP normal group compared with the BNP elevated and healthy groups (P-value < 0.001 for both). GATA3 demonstrated an auxiliary diagnostic utility for HFpEF with normal BNP levels, area under the receiver operating characteristic curve (AUC) = 0.77, P < 0.001, whereas IFNG exhibited a higher diagnostic value (AUC = 0.81, P < 0.001).Notably, IFNG and GATA3 were identified as potential molecular biomarkers for patients with HFpEF with normal BNP levels, highlighting their roles in the underlying inflammatory mechanisms of this distinct phenotype. - Source: PubMed
Wang XinyiJia KegangWang MengweiZhang YunqiangYe YingnanHou Ze - Nonseminomatous testicular germ cell tumors (NSE) present significant diagnostic challenges, especially for the early detection of serum tumor marker (STM) negative cases. Current diagnostic tools are limited, highlighting the need for innovative approaches. This study investigates a novel multi-analyte approach combining circulating cell-free DNA (cfDNA) and N-glycan profiling in both blood and seminal plasma to improve NSE diagnostics. - Source: PubMed
Publication date: 2025/07/11
Krasic JureSoic DinkoAbramovic Lucija SkaraKolosnjaj IvonaTomic MiroslavVrtaric AlenOguic Sasa KralikGelo NinaBojanac Ana KatusicJezek DavorMitrecic DinkoUlamec MonikaKulis TomislavGornik OlgaSincic Nino - Black patients with colon cancer (CC) exhibit more aggressive tumor biology and higher treatment resistance than white patients, even after adjusting for clinical and demographic factors. We investigated stage-specific transcriptional differences in tumor profiles of Black and white patients with CC. - Source: PubMed
Publication date: 2024/11/23
El Moheb MohamadShen ChengliKim SusanPutman KristinZhang HongjiRuff Samantha MWitt RussellTsung Allan - Spermiogenesis is considered to be crucial for the production of haploid spermatozoa with normal morphology, structure and function, but the mechanisms underlying this process remain largely unclear. Here, we demonstrate that SPEM family member 2 (Spem2), as a novel testis-enriched gene, is essential for spermiogenesis and male fertility. Spem2 is predominantly expressed in the haploid male germ cells and is highly conserved across mammals. Mice deficient for Spem2 develop male infertility associated with spermiogenesis impairment. Specifically, the insufficient sperm individualization, failure of excess cytoplasm shedding, and defects in acrosome formation are evident in Spem2-null sperm. Sperm counts and motility are also significantly reduced compared to controls. In vivo fertilization assays have shown that Spem2-null sperm are unable to fertilize oocytes, possibly due to their impaired ability to migrate from the uterus into the oviduct. However, the infertility of Spem2 males cannot be rescued by in vitro fertilization, suggesting that defective sperm-egg interaction may also be a contributing factor. Furthermore, SPEM2 is detected to interact with ZPBP, PRSS21, PRSS54, PRSS55, ADAM2 and ADAM3 and is also required for their processing and maturation in epididymal sperm. Our findings establish SPEM2 as an essential regulator of spermiogenesis and fertilization in mice, possibly in mammals including humans. Understanding the molecular role of SPEM2 could provide new insights into future therapeutic treatment of human male infertility and development of non-hormonal male contraceptives. - Source: PubMed
Publication date: 2024/02/29
Li ChaojieShen ChunlingXiong WenfengGe HaoyangShen YanChi JunZhang HongxinTang LingyunLu ShunyuanWang JinjinFei JianWang Zhugang