HRSP12 Blocking Peptide
- Known as:
- HRSP12 Blocking Peptide
- Catalog number:
- 33r-6500
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- HRSP12 Blocking Peptide
Related genes to: HRSP12 Blocking Peptide
- Gene:
- RIDA NIH gene
- Name:
- reactive intermediate imine deaminase A homolog
- Previous symbol:
- HRSP12
- Synonyms:
- UK114, P14.5, PSP
- Chromosome:
- 8q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-03
- Date modifiied:
- 2016-10-05
Related products to: HRSP12 Blocking Peptide
Related articles to: HRSP12 Blocking Peptide
- Ductal carcinoma in situ (DCIS) is a non-invasive precursor to invasive breast cancer. DCIS incidence continues to rise, yet its clinical management remains constrained by the absence of reliable biomarkers that can adequately distinguish indolent lesions from those with high invasive potential, to circumvent over- or under-treatment. Black women with DCIS are significantly more likely to progress to invasive breast cancer, are disproportionately diagnosed with high-grade, hormone receptor-negative lesions, and experience elevated risk of recurrence and mortality relative to White women with DCIS. These disparities persist despite comparable access to screening and treatment, suggesting underlying biological and tissue microenvironmental factors. This review synthesizes emerging evidence implicating early molecular and systemic changes that may be driving the disparity in DCIS progression. We highlight racial distinctions in interconnected pathways involving Wnt/β-catenin signaling, metabolic and nutritional dysregulation, immune microenvironment remodeling, and cellular tolerance of genomic instability. We further discuss how epigenetic alterations, obesity-associated inflammation, and immune dysregulation may arise during the pre-invasive stage that intersect with social and environmental exposures to influence racial differences in lesion fate. We spotlight candidate biomarkers disproportionately associated with aggressive disease in Black women-including KIFC1, a mediator of centrosome clustering and genomic instability tolerance, and ACKR1/DARC, a regulator of chemokine gradients and immune trafficking-as potential drivers of progression-permissive states. This review advances an integrated, equity-informed framework for DCIS progression that links early tumor evolution to coordinated alterations in genomic instability, immune regulation, metabolic signaling, and stress-adaptive pathways. Importantly, we propose that DCIS progression is governed not by isolated molecular alterations but by coordinated programs that enable survival under genomic and immunologic stress. Current clinical risk assays, which primarily capture tumor-intrinsic proliferation and hormone signaling, do not fully resolve these pathways and may therefore incompletely reflect biologically meaningful racial disparities. This synthesis underscores the need for pathway-level, microenvironment-informed, and population-representative approaches to DCIS risk stratification. Advancing such frameworks will be essential for identifying actionable biomarkers, refining early intervention strategies, and ultimately reducing racial disparities in breast cancer outcomes. - Source: PubMed
Publication date: 2026/05/31
Franklin DanaRida PadmashreeJinna Nikita - Misfolding of the cellular prion protein (PRP) is associated with fatal neurodegenerative prion diseases for which no treatments are currently available. Although the immune system is generally non-responsive (tolerant) to self-proteins such as PRP, evidence of anti-prion antibodies suggests escape from self-tolerance in some individuals and supports the potential for the human immune system to be leveraged against prion disease. Human leukocyte antigen (HLA) plays a central role in rejecting endogenous non-self proteins (e.g. cancer neoantigens) by activating CD8+ cytolytic T cells via the Class I system (HLA-I) and CD4+ helper T cells via the Class II (HLA-II) system. Here we investigated the predicted binding affinity of 334 HLA molecules with all possible linear 9-mer (for HLA-I) and 15-, 18- and 22-mer (for HLA-II) PRP peptides to identify peptide-HLA (pHLA) complexes with strong predicted binding (IC < 50 nM). We found that 12.4% of all prion peptides tested showed strong binding affinity to HLA molecules and that 20.2% of HLA alleles were able to bind strongly with PRP peptides. These findings suggest that carriers of certain HLA alleles that are capable of binding strongly to PRP peptides may have enhanced protection against prion disease, through reduction in the overall amount of PRP available for conversion to the misfolded, infectious scrapie isoform (PRP) of PRP and, potentially, by destroying it. These findings have implications for other disorders including common neurodegenerative diseases characterized by protein misfolding (e.g. α-synuclein, huntingtin, amyloid, tau, etc.). - Source: PubMed
Georgopoulos Apostolos PJames Lisa MSanders Matthew - Post-COVID-19 Syndrome (PCS) is characterised by persistent fatigue, cognitive impairments, and affective symptoms, yet its underlying neural mechanisms remain poorly understood. While static neuroimaging studies have identified resting-state connectivity abnormalities in PCS, such approaches fail to capture the brain's dynamic functional organisation. This represents a missed opportunity to understand how alterations in large-scale network interactions may contribute to the fluctuating symptom profile of PCS. Cognitive and emotional processes rely on the brain's capacity to flexibly reconfigure large-scale networks over time; disruptions in this dynamic repertoire may therefore play a role in PCS pathophysiology. - Source: PubMed
Publication date: 2026/05/25
Cahart Marie-StephanieO' Daly OwenCai ZiyuanMariani NicoleBorsini AlessandraMondelli ValeriaEiff BrandiRota SilviaNicholson TimothyRida LailaHampshire AdamDipasquale OttaviaFernandes LiaTurkheimer FedericoWilliams Steven C RMartins Daniel - Identifying reliable biomarkers for prion diseases remains a challenge, particularly for early detection in accessible body fluids. A recent mass spectrometry study on the cerebrospinal fluid proteome identified and validated five proteins significantly dysregulated in the preclinical stage of naturally scrapie-affected sheep. In this study, we quantified these proteins in serum and analysed their distribution and gene expression in the central nervous system, correlating these results with characteristic prion-related neuropathological features. Significantly elevated serum levels of synaptotagmin binding, cytoplasmic RNA interacting protein (SYNCRIP), phospholipase D3 (PLD3) and cathepsin D (CTSD) were detected in preclinical animals, mirroring previous cerebrospinal fluid findings. Central nervous system analyses on these three proteins together with osteopontin (SPP1) and complement component 4 (C4) revealed early and region-specific reduced immunoreactivity alongside upregulated gene expression in scrapie-affected animals, correlating significantly with prion-associated neuropathological features. Together, these findings highlight the potential of SYNCRIP, PLD3 and CTSD as promising minimally invasive biomarkers to diagnose prion diseases from the preclinical stage and provide new insights into the spatiotemporal regulation of the five proteins in the central nervous system throughout the progression of disease. Further research is needed to clarify the peripheral biomarker dynamics in relation to the neurodegenerative pathology. - Source: PubMed
Publication date: 2026/06/02
Pérez-Lázaro SoniaBarrio TomásSevilla EloisaBolea RosaBadiola Juan J - Long COVID is increasingly recognized as a complex multisystem condition, with brain fog and cognitive impairment emerging as some of its manifestations. Despite growing literature, the pooled prevalence, subgroup differences, and underlying mechanisms remain incompletely understood. - Source: PubMed
Faseeh AhmarRida MaryamKarim Noor EZafar AyeshaShah ArifPerveen Abida