PHLDA1 Antibody (N-term) Blocking Peptide
- Known as:
- PHLDA1 Antibody (N-terminus) Blocking Peptide
- Catalog number:
- BP18855a
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- PHLDA1 Antibody (N-term) Blocking Peptide
Related genes to: PHLDA1 Antibody (N-term) Blocking Peptide
- Gene:
- PHLDA1 NIH gene
- Name:
- pleckstrin homology like domain family A member 1
- Previous symbol:
- -
- Synonyms:
- TDAG51, DT1P1B11, PHRIP
- Chromosome:
- 12q15
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-19
- Date modifiied:
- 2016-01-27
Related products to: PHLDA1 Antibody (N-term) Blocking Peptide
Related articles to: PHLDA1 Antibody (N-term) Blocking Peptide
- Head and neck squamous cell carcinoma (HNSC) is a leading cause of morbidity and mortality worldwide. The roles of PHLDA genes in HNSC progression remain unclear. This study explores their expression, mutational landscape, and functional roles as potential diagnostic biomarkers and therapeutic targets. Eight HNSC cell lines and six normal oral keratinocyte cell lines were cultured, and RNA extraction and RT-qPCR analysis were conducted. The GSCA database validated gene expression in clinical HNSC samples. Methylation and survival analysis were performed using TCGA data, with survival correlation assessed via the KM Plotter tool and UALCAN database. Mutational analysis was done via cBioPortal, and immune-related correlations were analyzed using TISIDB. Functional assays were performed after siRNA-mediated knock down of PHLDA genes in SCC9 and SCC25 cells, including Western blot, CCK-8, colony formation, and wound healing assays. Our results demonstrate that PHLDA1, PHLDA2, and PHLDA3 are significantly upregulated in HNSC cell lines compared with normal controls, with PHLDA1 showing the most substantial increase. ROC analysis revealed that PHLDA1 exhibited the highest diagnostic potential for distinguishing HNSC from normal tissues. Methylation analysis showed hypomethylation of PHLDA genes in tumor tissues, particularly in the promoter regions. Higher expression of PHLDA genes correlated with poorer overall survival outcomes in HNSC patients. Mutational analysis revealed that PHLDA2 exhibited the highest mutation rate, with predominantly missense mutations. The PPI network analysis indicated that PHLDA genes interact with several cancer-related proteins, and DAVID analysis showed their involvement in processes like cell cycle regulation and tumorigenesis. Functional assays demonstrated that silencing of PHLDA genes in HNSC cells significantly impaired cell proliferation, clonogenic potential, and migration, suggesting their role as oncogenic regulators. Our study identifies PHLDA1, PHLDA2, and PHLDA3 as potential diagnostic biomarkers and therapeutic targets in HNSC. These genes are involved in critical pathways related to cancer progression and immune modulation. The findings suggest that targeting PHLDA genes may provide a novel approach for overcoming therapeutic resistance and improving patient outcomes in HNSC. - Source: PubMed
Publication date: 2026/05/26
Abdel-Maksoud Mostafa AAlamri AbdulazizFahad AljawharahAlrokayan SalmanAufy MohammedKiani Bushra HafeezZhang HanyongAyaz Muhammad MazharHameed YasirAlmutairi Saeedah - Herpesviruses infect nearly all humans and have long been implicated in autoimmune and chronic diseases, yet their immune interactions with host proteins have not been systematically characterized at population scale. We profiled immunoglobulin G reactivities to >4,600 herpesvirus peptides and >15,000 human proteins using multiplexed protein display in two Mass General Brigham Biobank cohorts (discovery n=1,289; replication n=763), with longitudinal electronic health record follow-up. We identified and replicated 3,943 FDR-significant associations across 93 autoantigens, including previously uncharacterized viral-autoantigen axes, such as PHLDA1 and ZNF550. Eleven autoantigens were predicted by viral peptide reactivities with >85% accuracy in independent validation; some exhibited shared viral-host sequence homology, consistent with possible molecular mimicry. Integrating immune reactivities with incident disease outcomes revealed virus-specific network architectures: cytomegalovirus formed the largest multimorbid network, Epstein-Barr virus converged on pleiotropic autoimmune hubs, and herpes simplex viruses formed smaller, partially overlapping autoreactive networks. These findings define a herpesvirus-autoantigen-disease network atlas and prioritize candidate viral-host immune axes for mechanistic investigation. - Source: PubMed
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