HIV protease
- Known as:
- H. sapiens immunodeficiency virus protease
- Catalog number:
- 10-302-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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- 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 - 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 - [This corrects the article DOI: 10.3389/fgene.2026.1776779.]. - Source: PubMed
Publication date: 2026/07/08
Sannan Naif S - Cerebral small vessel diseases (CSVDs) are a group of disorders affecting the small arteries, veins, and capillaries supplying the white matter and deep grey matter structures. They are the most common form of cerebrovascular disease, accounting for approximately half of vascular dementia cases and 20% of stroke incidence. Whilst genetic testing is a routine diagnostic tool for monogenic CSVDs, less than 20% of patients have a causal variant in known CSVD genes. We performed whole exome sequencing on 117 patients suspected of monogenic CSVD who previously tested negative for pathogenic variants in seven well-characterised CSVD genes (NOTCH3, HTRA1, COL4A1, COL4A2, TREX1, GLA, and FOXC1). Targeted analysis was conducted on known and associated CSVD genes, as well as candidate genes which cause conditions with overlapping symptomology to CSVD. Burden analysis focussing on rare, functional variants was used to identify novel associations when compared against a cohort of 1035 non-neurological controls. We identified 18 suspected disease-causing variants across nine CSVD-associated genes and a significant burden of both rare and rare, likely disease-causing heterozygous variants in ABCC6. Two genes from stroke and neurodegenerative disease gene panels also possessed a significant burden of rare, likely disease-causing variants, MYH11 (adjusted P = 1 × 10) and NOTCH1 (adjusted P = 1 × 10). We further identified novel associations for seven genes (COL7A1, HMCN1, LAMA1, MMP9, TENM4, TNC, TTN) with monogenic CSVD in this cohort. Our findings implicate several genes as potentially causal of monogenic CSVD, highlighting the need for more extensive genetic screening in suspected CSVD cases, and functional characterisation of implicated variants to determine their mechanistic role in CSVD pathogenesis. - Source: PubMed
Publication date: 2026/07/21
Guyler Solomon KAlfayyadh Mohammed MMaksemous NevenLea Rodney ASmith Robert ASutherland Heidi GGriffiths Lyn R - Alzheimer's disease (AD) and cerebrovascular pathology are the two most common causes of dementia, frequently co-occurring in older people. Community-based neuropathology studies indicate that vascular disease accounts for approximately one-third of the population-attributable risk of dementia, controlling for other pathologies (including AD). The proportion with vascular disease as co-pathology is likely to be higher (50-70%). The most common vascular substrate is cerebral small vessel disease, which includes small artery fibrosis (arteriolosclerosis), vascular amyloid deposits (cerebral amyloid angiopathy), and monogenic forms of small vessel disease, the commonest being Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL). Post-stroke cognitive impairment following both ischemic stroke and intracerebral hemorrhage also contributes. - Source: PubMed
Publication date: 2026/07/15
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