RECOMBINANT HEPATITIS B 320 CORE ANTIGEN 18kDa AYW, Product Type Recombinant Protein, Specificity HEPATITIS B 320 CORE ANTIGEN, Target Species Viral, Host N_A, Format Rec. Protein, Isotypes , Ap
- Known as:
- RECOMBINANT HEPATITIS B 320 CORE ANTIGEN 18kDa AYW, Product Type Recombinant Protein, Specificity HEPATITIS B 320 CORE ANTIGEN, Target Species Viral, Host N_A, Format Rec. Protein, Isotypes , Ap
- Catalog number:
- 0200-0085
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- AbD
- Gene target:
- RECOMBINANT HEPATITIS 320 CORE ANTIGEN 18kDa AYW Product Type Recombinant Protein Specificity Target Species Viral Host N_A Format Rec. Isotypes
Related genes to: RECOMBINANT HEPATITIS B 320 CORE ANTIGEN 18kDa AYW, Product Type Recombinant Protein, Specificity HEPATITIS B 320 CORE ANTIGEN, Target Species Viral, Host N_A, Format Rec. Protein, Isotypes , Ap
- Gene:
- RCOR1 NIH gene
- Name:
- REST corepressor 1
- Previous symbol:
- RCOR
- Synonyms:
- COREST, KIAA0071
- Chromosome:
- 14q32.33
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-09
- Date modifiied:
- 2016-04-25
- Gene:
- REC8 NIH gene
- Name:
- REC8 meiotic recombination protein
- Previous symbol:
- REC8L1
- Synonyms:
- Rec8p, kleisin-alpha
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-29
- Date modifiied:
- 2016-01-15
- Gene:
- RECQL NIH gene
- Name:
- RecQ like helicase
- Previous symbol:
- -
- Synonyms:
- RecQ1, RecQL1
- Chromosome:
- 12p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-03-25
- Date modifiied:
- 2016-02-05
- Gene:
- RECQL4 NIH gene
- Name:
- RecQ like helicase 4
- Previous symbol:
- -
- Synonyms:
- RecQ4
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-06
- Date modifiied:
- 2019-04-23
- Gene:
- RECQL5 NIH gene
- Name:
- RecQ like helicase 5
- Previous symbol:
- -
- Synonyms:
- RecQ5, FLJ90603
- Chromosome:
- 17q25
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-06
- Date modifiied:
- 2016-02-05
Related products to: RECOMBINANT HEPATITIS B 320 CORE ANTIGEN 18kDa AYW, Product Type Recombinant Protein, Specificity HEPATITIS B 320 CORE ANTIGEN, Target Species Viral, Host N_A, Format Rec. Protein, Isotypes , Ap
Related articles to: RECOMBINANT HEPATITIS B 320 CORE ANTIGEN 18kDa AYW, Product Type Recombinant Protein, Specificity HEPATITIS B 320 CORE ANTIGEN, Target Species Viral, Host N_A, Format Rec. Protein, Isotypes , Ap
- Fragile X-associated Tremor/Ataxia Syndrome (FXTAS) is a late-onset neurodegenerative disorder caused by FMR1 premutation CGG repeat expansions (55-200 repeats). The epigenetic landscape of the FXTAS brain remains uncharacterized. We performed genome-wide DNA methylation profiling of postmortem prefrontal cortex tissue to identify differentially methylated positions (DMPs) and candidate genes, and sought protein-level support for a neuroinflammatory signal. - Source: PubMed
Publication date: 2026/07/10
Lozano ReymundoLin XiaoHagerman RandiCerdeño Verónica MartínezPinto Dalila - SNAIL is a transcription factor that plays a role in development and cancer. SNAIL contains an N-terminal SNAG domain that is a high-affinity ligand for the histone substrate binding lysine-specific demethylase 1 (LSD1). SNAIL also contains a C-terminal zinc finger domain that binds to DNA E-box sequences. SNAIL and related transcription factor family members are known to recruit LSD1-containing protein complexes to specific sites in chromatin to regulate gene expression. LSD1 can form a multiprotein complex with histone deacetylase 1 (HDAC1) and CoREST scaffolding protein (LHC). In this study, we use a purified system to analyze the role of SNAIL in modulating nucleosome deacetylation by the LHC complex. We find that SNAIL enhances nucleosome deacetylase activity of the LHC complex at multiple histone H3 sites through multivalent interactions. Enhanced nucleosome deacetylation is dependent on SNAIL's SNAG and zinc finger domains. Unexpectedly, we find that SNAIL-stimulated nucleosome deacetylation by LHC also involves interactions of the nucleosome histone acidic patch, including histone H2A acidic residues. Modeling and mutagenesis experiments suggest that this acidic patch could engage a basic patch in the disordered segment of LSD1. Together, these findings reveal how a transcription factor can influence a cascade of molecular recognition events to regulate chromatin structure. - Source: PubMed
Nam EunjuValeriano Manuel OsorioWang Zhipeng AWhedon Samuel DJiang HanjieZhang Maggie XinranDuBois-Coyne SarahHaque Ishraq AJiang JenniferFerreira JenniferFarnung LucasLee KwangwoonCole Philip A - Renal-resident macrophages (RMs) are essential regulators of kidney homeostasis and repair, yet the mechanisms governing RM niche regeneration after acute depletion remain poorly defined. To overcome these limitations, we have developed an inducible human CD59- intermedilysin (hCD59-ILY) ablation system, enabling rapid, specific, and reversible depletion of targeted macrophage populations, and subsequent replenishment of RMs, followed by longitudinal scRNA-seq analysis of kidneys at baseline and days 1, 3, and 7 post-ablation. RM ablation triggered a rapid and sustained upregulation of , predominantly in proximal tubular epithelial cells (PTC1/PTC2), establishing a persistent chemotactic niche signal that coincided with macrophage repopulation. Regenerating RMs transitioned from inflammatory/stress-associated states toward metabolically active and proliferative phenotypes enriched in glycolysis, oxidative phosphorylation, MYC, and cell-cycle programs, with attenuation of canonical inflammatory pathways. Cell-cell communication analysis revealed an early burst of intercellular signaling at day 1, followed by progressive normalization, with fibronectin ), osteopontin (), chemokine (), and amyloid precursor protein () axes emerging as key mediators of niche restoration. Transcriptional network analysis identified a conserved regulatory module (, , , , , ) coordinating macrophage differentiation and regenerative programming, linking metabolic adaptation to lineage reconstitution. Sub-clustering revealed five dynamically shifting RM subsets with distinct inflammatory, remodeling, proliferative, and surveillance states, reflecting a hierarchical regeneration process. Functional validation using clodronate-mediated depletion in Secreted Phosphoprotein 1 (Opn)-deficient mice demonstrated impaired macrophage repopulation, establishing osteopontin as a critical regulator of RM regeneration. Together, these data define a coordinated epithelial-immune circuit in which Cx3cl1-driven chemotaxis, -dependent signaling, and a core transcriptional network orchestrate macrophage niche reconstitution and kidney repair following acute immune cell ablation. - Source: PubMed
Publication date: 2026/06/18
Islamuddin MohammadJi LixuanChen YilinSong KejingEllsworth Calder RRappaport JackWang ChenxiaoLiu ShumeiKolls JayXu XiaojiangQin Xuebin - Cognitive impairment is a common yet under-recognised complication of ischaemic stroke (IS), with long-term effects on patient quality of life and rehabilitation outcomes. Identifying early biomarkers and protective factors such as cognitive reserve (CR) is essential for improving prognosis and guiding targeted interventions. This study aimed to determine the following: (i) RNA gene expression profiling during acute stroke and (ii) the associations between target genes as well as clinical factors and cognitive impairment during an acute event and at the 3-month follow-up. A three-month prospective cohort study involving 24 adults with mild to moderate IS and 24 age- and sex-matched controls admitted to Hospital Canselor Tuanku Muhriz, Malaysia, was conducted. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA) within 48 h of stroke and at 3 months. Peripheral blood samples were collected for RNA extraction, and gene expression was analysed using RT² Profiler PCR arrays. Cognitive reserve was measured using the Cognitive Reserve Index Questionnaire (CRI-q). Statistical analyses included chi-square and independent t tests. At baseline, 83.3% of IS patients exhibited cognitive impairment (mean age 64.6 ± 10.5 years). Increased age (p = 0.006), low education level (p = 0.010), diabetes mellitus (p = 0.010), CRI-Education (p = 0.010) and CRI-Working Activity (p = 0.009) were significantly associated with baseline cognitive impairment. These clinical and CR factors survived False Discovery Rate (FDR) correction at the baseline stage (p < 0.05). However, at the 3-month follow-up, no clinical or CR factors remained statistically significant after FDR correction. Regarding gene expression, while MAPK1 (p = 0.029) and CAPZB (p = 0.042) were nominally upregulated in patients, and RCOR1 (p = 0.043) showed a nominal association with baseline impairment, no genetic markers survived FDR correction at either time point. Age, diabetes, and cognitive reserve are robust determinants of cognitive status during the acute phase of ischaemic stroke. The loss of significance at 3 months suggests these factors are primary drivers of initial functional buffering rather than long-term recovery trajectories in this cohort. CR should be utilised as a prognostic stratification tool during admission to identify high-risk patients rather than as a direct target for acute intervention. Future large-scale studies are required to validate whether the observed nominal gene expression trends can serve as reliable biomarkers for long-term recovery. - Source: PubMed
Publication date: 2026/04/20
Muhamad Nurul NadiahKatijjahbe Md AliAbdul Murad Nor AzianWan Zaidi Wan AsyrafMohamed Saini Suriati - Microsporidia are known intracellular pathogens that infect nearly all animals and deeply manipulate host mitochondrial homeostasis for survival. Here, we report a novel mechanism by which the human-pathogenic Encephalitozoon hellem modulates the mitophagy machinery of its host. We identified the secreted protein EhPTP4 as a key effector in disrupting selective degradation processes in the infected cells. EhPTP4 is found to localize within the nucleus of infected cells, where it induces increased expression of endoplasmic reticulum-associated degradation (ERAD) pathway components, including HSPA5, HERPUD1, and PDIA4. This induction enhances protein ubiquitination in host cells and leads to the degradation of BNIP3L, a critical regulator of mitophagy. Investigation into the molecular interaction network revealed that EhPTP4 interacts with host corepressor RCOR1 and histone H3. This interaction modulates histone acetylation, specifically at H3K14ac sites, thereby further influencing the expression of a key ERAD gene, HERPUD1. This study uncovers a sophisticated strategy by which microsporidia manipulates both ER stress response and the histone acetylation to suppress mitophagy. These findings provide new insights into the mechanisms of microsporidian pathogenesis. - Source: PubMed
Publication date: 2026/03/23
Zou ZiyunHu YiboGuan ZhongxiaChen JiajingZhang QingyaoHan YinzeZhu JunyuWang ChunxiaHan BingLi TianZhou Zeyang