Ask about this productRelated genes to: HIF1AN protein
- Gene:
- HIF1AN NIH gene
- Name:
- hypoxia inducible factor 1 subunit alpha inhibitor
- Previous symbol:
- -
- Synonyms:
- FLJ20615, DKFZp762F1811, FLJ22027, FIH1
- Chromosome:
- 10q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-27
- Date modifiied:
- 2018-04-23
Related products to: HIF1AN protein
Related articles to: HIF1AN protein
- Natural products (NPs) are a major source of bioactive molecules for drug discovery, yet their development and translation are often limited by inefficient and ambiguous target identification. Although mass spectrometry-based proteomics has advanced rapidly, upstream sample preparation remains a critical bottleneck for high-throughput target deconvolution. Here, we report μPAS (micro proteomics automation system), an automated and miniaturized proteomic sample preparation platform that integrates protein reduction, alkylation, digestion, and TMTpro labeling into a single streamlined workflow. By achieving a 3- to 7-fold reduction in digestion and labeling volumes, μPAS improves throughput and cost efficiency, reducing TMT reagent consumption by 2-7.5-fold while maintaining high digestion efficiency (>90% within 4 h) and TMTpro labeling efficiency (>96%). The platform demonstrates consistent intra- and inter-batch reproducibility, with Pearson correlation coefficients exceeding 0.96. Using three model compounds, μPAS was benchmarked against three complementary target identification strategies, enabling automated target discovery. Application of μPAS to a 96-sample workflow enabled systematic target deconvolution for 18 NPs lacking well-defined targets. Key candidate targets, including HIF1AN, FECH, and TXNRD1, were further validated using Western blot-based thermal shift assays, confirming target engagement. Collectively, these results establish μPAS as a robust and scalable platform for high-throughput NP target discovery, facilitating mechanistic elucidation of NP bioactivity. - Source: PubMed
Publication date: 2026/05/18
Wu QiongLin YueChen JiayiLiao BinQiu XianjieLu YongzhiXi ShuangtongDai MinxianWu KunzhongLi WenqiHuang WenhuiTang MiruShang Jinsai - Postmenopausal osteoporosis (PMOP) is characterized by exacerbated bone resorption and inadequate bone formation, with macrophage-driven inflammation playing a key role. However, how immunometabolic reprogramming of macrophages modulates osteoblast fate remains unknown. - Source: PubMed
Publication date: 2026/05/03
Gu YifanWang KunWang YicongWang ZiruLi YihengLi LeiJiang ShuaiZheng YuFeng RunYang Min - Accurate prediction of peptide-protein interactions (PepPI) is crucial for advancing peptide-based anticancer drug design. In this study, we introduce ProVenTL, a computer-aided molecular design framework that leverages transfer learning and protein language model embeddings to enhance PepPI prediction accuracy and interpretability. Two complementary strategies were explored: (i) fine-tuning a CAMP model pretrained on large-scale PepPI data from the Protein Data Bank (PDB) using a curated dataset of Calloselasma rhodostoma venom peptides and cancer-related proteins, and (ii) integrating ProtT5 embeddings with stacked autoencoder-deep neural networks (SAE-DNN) and TabNet classifiers. Models were comprehensively benchmarked against baseline configurations and representative deep-learning approaches using standard classification metrics, while biological relevance was evaluated through functional enrichment and pathway analysis of top-ranked predictions. Compared with baseline configurations and conventional deep-learning approaches, the ProtT5-based SAE-DNN model achieved the best performance (accuracy = 0.78; ROC-AUC = 0.86), demonstrating improved generalization capability on a small, domain-specific venom peptide dataset. The model identified key targets such as TRBC2, CD274, HIF1AN, PCSK9, and PLAU, which are associated with pathways involved in immune suppression, hypoxia regulation, lipid metabolism, and metastasis. This study highlights the utility of transfer learning and protein language models for PepPI prediction in data-limited scenarios and establishes a computational framework for prioritizing snake-venom-derived peptides for anticancer drug discovery and future experimental validation. - Source: PubMed
Publication date: 2026/04/02
Adhiva JeniPradana Hanif AdityaKusuma Wisnu AnantaHaryanto TotoAmanda Chairunnisa NurSofyantoro FajarYudha Donan SatriaNuringtyas Tri RiniPutri Wahyu AristyaningPurwestri Yekti AsihLischer KennySwasono Respati Tri - Esophageal cancer (EC) is a rapidly progressing malignancy that significantly contributes to cancer-related mortality. The genetic causes of EC, particularly rare coding pathogenic variants, remain incompletely defined. This study focuses on non-synonymous single nucleotide polymorphisms (nsSNPs) because they can impact the functions of critical proteins implicated in carcinogenesis. - Source: PubMed
Publication date: 2026/02/23
Azmi Muhammad BilalQureshi SajidaWasi RafiaNiaz Saad KhalidAhmed Syed Danish Haseen - Neuroendocrine prostate cancer (NEPC) is a highly aggressive subtype of prostate cancer (PCa), associated with poor prognosis and resistance to androgen receptor (AR)‑targeted therapies. Hypoxia is a well‑established driver of lineage plasticity and has been implicated in promoting NE differentiation (NED) of tumors. However, the underlying molecular mechanisms linking hypoxia to NED remain unclear. In the present study, miR‑135b‑5p was identified as a critical regulator of hypoxia‑induced NED through modulation of the hypoxia‑inducible factor alpha‑1 subunit alpha inhibitor (HIF1AN)‑HIF1α axis. Exposure of androgen‑dependent PCa cell lines (LNCaP and VCaP) to hypoxia induced neurite outgrowth and increased expression of NE markers, concurrent with upregulation of miR‑135b‑5p. Target prediction followed by experimental validation in luciferase reporter assays confirmed that HIF1AN is a direct target of miR‑135b‑5p. Suppression of HIF1AN results in the stabilization of HIF1α, which in turn activates the AKT/mTOR signaling pathway, facilitating NE trans differentiation. Functional studies demonstrated that overexpression of miR‑135b‑5p by mimics promotes NED in LNCaP cells, while inhibition of miR‑135b‑5p reverses the NE features in NE‑LNCaP and NCI‑H660, NE cells. Furthermore, pharmacological inhibition of HIF1α using PX‑478 abrogated hypoxia‑induced NED and attenuated activation of AKT/mTOR signaling, further underscoring the significance of the miR‑135b‑5p‑HIF1AN‑HIF1α axis in NED of PCa cells. Collectively, the findings of the present study reveal a novel miR‑135b‑5p‑HIF1AN‑HIF1α signaling axis that is involved in hypoxia‑induced NED via AKT/mTOR activation and identify miR‑135b‑5p and HIF1α as potential therapeutic targets for NEPC. - Source: PubMed
Publication date: 2026/02/20
Lakshmi Pampana Sandhya VenkataParashar JagratiBiswas BiswajitUmmanni Ramesh