HIV protease
- Known as:
- H. sapiens immunodeficiency virus protease
- Catalog number:
- 11-302-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- HIV protease
Related genes to: HIV protease
- Gene:
- HTRA1 NIH gene
- Name:
- HtrA serine peptidase 1
- Previous symbol:
- PRSS11
- Synonyms:
- HtrA, IGFBP5-protease, ARMD7
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-25
- Date modifiied:
- 2016-10-05
Related products to: HIV protease
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- Cerebral small vessel disease (CSVD) describes a range of neurological diseases affecting the small arteries, veins, and capillaries which supply the white matter and deep grey matter structures of the brain. They are the most common form of cerebrovascular disease, accounting for almost half of vascular dementia cases and approximately 20% of stroke incidence globally. Genetic testing is a routine diagnostic tool for monogenic CSVDs; however, less than 20% of patients have a causal variant in a known gene. Genetic testing for these disorders focuses on single nucleotide variants and short insertions or deletions, with larger genomic variation often unexplored as a cause of disease. In this study we performed whole-exome sequencing (WES) on 111 patients suspected of familial CSVD that had previously tested negative for pathogenic variants in seven known CSVD genes (NOTCH3, HTRA1, COL4A1, COL4A2, TREX1, GLA, and FOXC1). Bioinformatic analysis of WES data, multiplex ligation-dependent probe amplification, quantitative real-time polymerase chain reaction assays, and Nanopore long-read sequencing were used to identify suspected copy number variants. This work identified four candidate CNVs across NOTCH3, LMNB1, and COL4A2 which are potential causes of CSVD and highlights the need for further investigation of more complex forms of genetic variation and their potential roles as causal of CSVD. - Source: PubMed
Publication date: 2026/08/27
Guyler Solomon KMaksemous NevenLea Rodney ASmith Robert ASutherland Heidi GGriffiths Lyn R - A peripheral nerve sheath tumour composed predominantly of Wagner-Meissner (W-M) bodies is typically regarded as a variant of schwannoma and has been considered rare. Interestingly, a SH3PXD2A::HTRA1 fusion was found which is described in schwannomas with a so-called "serpentine" palisading pattern comprising short palisades of Schwann cells. - Source: PubMed
Publication date: 2026/08/26
Wilsher Mark JamesBerber Onur - The vascular system is the largest organ in the body and underlies most chronic diseases, yet the molecular mechanisms that govern its plasticity remain poorly defined. - Source: PubMed
Publication date: 2026/08/13
Amrute Junedh MJiang LihuaBolar NikhitaHiga KellyZhu ChenchenJian RuiqiKim JenniferDuda MatthewPuaala Anna MarieKlinder AvaniDalal AlexPedroza AlbertReinhardt Dieter PCheng PaulSnyder MichaelFischbein Michael P - Age-related macular degeneration (AMD) is a complex disease wherein age, genetics, and environment play a role. How each of these factors contribute to the overall disease initiation and progression remains largely unelucidated. A renewed examination of the existing literature regarding the blood supply to the outer retina may provide novel insights. Hypoxia in the retinal pigment epithelium (RPE) can produce features of AMD, including photoreceptor degeneration. In the macula, the choriocapillaris has unique features making it susceptible to hypoperfusion, producing low-grade ischemia and chronic tissue hypoxia. The choriocapillaris experiences vascular loss and decreased blood flow early in AMD. Genetic risk, when viewed through a new lens, points to vascular insult as central to AMD pathophysiology. Complement-related risk genes are active in the vasculature, from large tributary vessels to small vessels of the choriocapillaris. HtrA serine peptidase 1 (HTRA1) is associated with cerebral small vessel disease and localizes to the choriocapillaris in AMD. Ageing can be interpreted as inevitable atherosclerosis from large to small vessels of the cerebral system. Western diets, smoking, and a rising prevalence of metabolic syndrome in people over age 60 are confirmed to accelerate both atherosclerosis and AMD. A perfusion-based model for complement-related, soft drusen-associated AMD is proposed while also explaining a second phenotype of non-complement related subretinal drusenoid deposit-associated AMD. Common to both phenotypes of AMD is chronic hypoperfusion causing decreased oxygen exchange and waste removal at the neurovascular unit of the choriocapillaris, RPE, and photoreceptors. Understanding AMD as an end-organ vascular disease may move us towards a unifying hypothesis. - Source: PubMed
Publication date: 2026/08/05
Holekamp Nancy MIvanova Simona Ivanova - associated stomach adenocarcinoma (STAD) represents a highly severe malady, with up to 1 million new cases annually. Here, we examined novel human and bacterial risk determinants as well as related signal transduction events associated with STAD development. serine protease HtrA cleaves the junctional protein E-cadherin, which results in the disruption of epithelial cell connections, the release and nuclear accumulation of β-catenin, and the onset of epithelial-mesenchymal transition (EMT), a hallmark of many tumors. In addition, the injection of oncoprotein CagA into host epithelial cells targets β-catenin-mediated cell proliferation and other cancer signaling pathways. By analyzing over 2,000 genomes, we identified single-nucleotide polymorphism (SNP) variants of HtrA and CagA that are associated with STAD progression. In addition, we investigated the role of the human serine proteases HTRA1, HTRA2, HTRA3, and HTRA4 in STAD progression and linked the genetic and expression data with specific signaling pathways. Elevated HTRA1, HTRA2, and HTRA3 expression in STAD patients correlated with upregulated extracellular matrix (ECM) receptor interactions and signaling that are critical for EMT. Moreover, positive STAD patients exhibited increased epithelial cell signaling, chronic inflammation, transcription factor Wnt/β-catenin signaling, ECM damage and metastasis, and single-cell analyses showed a strong association between HTRA1, the receptor Wnt, β-catenin, and oncogene MYC expression. Analyses of mutations in human HTRA1 and HtrA revealed a role in the up- or downregulation of STAD progression. Together, our data show that SNPs in human and serine protease HtrA and CagA modulate cancer signaling in complex Wnt-/β-catenin and ECM signaling networks, and that the protein variants can be causative or protective factors. A signaling model is proposed that highlights the complex interplay of human and bacterial factors in critical tumor signaling events, which could serve as predictive STAD biomarkers in patients. - Source: PubMed
Publication date: 2026/07/23
Linz BodoRajaratnam SaiswaroopTegtmeyer NicoleChhetri AakashGunanathan KrishnasaliniKanchi SubbaraoPachathundikandi Suneesh KumarSivaramakrishnan VenketeshBackert Steffen