LRIG1 | Lig-1 | Blocking peptide
- Known as:
- LRIG1 | Lig-1 | Blocking short protein sequence
- Catalog number:
- as06148p
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Agrisera
- Gene target:
- LRIG1 | Lig-1 Blocking peptide
Related genes to: LRIG1 | Lig-1 | Blocking peptide
- Gene:
- LIG1 NIH gene
- Name:
- DNA ligase 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1991-05-09
- Date modifiied:
- 2019-04-23
- Gene:
- LRIG1 NIH gene
- Name:
- leucine rich repeats and immunoglobulin like domains 1
- Previous symbol:
- -
- Synonyms:
- LIG-1, DKFZP586O1624, LIG1
- Chromosome:
- 3p14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-23
- Date modifiied:
- 2016-10-05
Related products to: LRIG1 | Lig-1 | Blocking peptide
Related articles to: LRIG1 | Lig-1 | Blocking peptide
- Epidermal growth factor receptor signaling maintains intestinal homeostasis by modulating proliferation and differentiation within the stem cell compartment, with excess epidermal growth factor receptor signaling predisposing to neoplasia. Epidermal growth factor receptor protein levels are central to epidermal growth factor receptor function. These levels are negatively regulated by leucine-rich repeats and immunoglobulin-like domains 1, which accelerates receptor internalization and degradation, supporting a tumor suppressor role for leucine-rich repeats and immunoglobulin-like domains 1. Leucine-rich repeats and immunoglobulin-like domains 3 is a less-studied family member that has been reported, in a context-dependent manner, to both cooperate with and oppose the effects of leucine-rich repeats and immunoglobulin-like domains 1 on epidermal growth factor receptor. - Source: PubMed
Publication date: 2026/08/31
Bechard Matthew EChen ZhengyiZhao PingAramandla RadhikaYang YilinSimmons Alan JWashington M KayFranklin Jeffery LLau Ken SCoffey Robert J - Dementia with Lewy Bodies (DLB) is the most common neurodegenerative dementia after Alzheimer's disease (AD), but it remains challenging to diagnose due to overlapping symptoms and mixed pathologies. This pilot study tested whether DLB has different metabolic blood proteomic profiles compared to AD and controls. Serum was analysed from people with DLB ( = 20), a group with AD (either with Alzheimer's disease dementia or Mild Cognitive Impairment with a positive amyloid positron emission tomography scan (MCI+/AD) ( = 15), and similarly aged controls ( = 15) using the Olink Metabolism panel encompassing 92 proteins. Six proteins (PILRB, LRIG1, NECTIN2, TINAGL1, SSC4D, and FKBP4) were significantly different in DLB compared with the controls, and one protein (SERPINB8) was differentially expressed when compared with MCI+/AD. Receiver operating characteristic curves for biologically relevant proteins that have previously established roles in neurodegenerative and cognitive properties showed that RNASE3 levels could differentiate DLB from MCI+/AD (area under the curve (AUC) = 0.717, sensitivity = 0.850, and specificity = 0.600). A multimarker model incorporating RNASE3 with phosphorylated tau 217 (pTau217) and polygenic risk scores for LBD achieved improved accuracy in discriminating DLB from MCI+/AD (AUC = 0.963, sensitivity = 1.000, and specificity = 0.900). Pathway analyses revealed dysregulation in cortisol signalling, inflammation resolution, and ErbB4-mediated neuroplasticity, which point towards peripheral protein alterations related to the adaptation to stress, immune regulation, and synaptic integrity in DLB. The present exploratory study highlights potential pathophysiological mechanisms implicated in DLB, suggesting that a multimodal biomarker panel may perform better compared to single proteins. Considering the small sample sizes, the findings will need to be replicated in larger cohorts. - Source: PubMed
Publication date: 2026/07/31
Pritha Ariana NChouliaras LeonidasSwann PeterPrats-Sedano MariaMcKeever AnnaHeslegrave AmandaAshton Nicholas JZetterberg HenrikSu LiMalpetti MauraRowe James BO'Brien John T - In humans, 2,3,7,8-tetrachlorodibenzo--dioxin (TCDD) induces chloracne, a skin condition that presents with acanthosis, hyperkeratosis, comedones, and sebaceous gland (SG) atrophy (seboatrophy). Although chloracne-like phenotypes have been reported in TCDD-treated mice, the underlying mechanisms remain poorly understood. Previous studies showed that TCDD-induced CYP1A1 protein is expressed in LRIG1+ progenitor cells in hair follicles, suggesting that TCDD targets specific cell populations within the pilosebaceous unit. To explore the effects of TCDD on the epidermis and pilosebaceous unit, we analyzed single-cell RNA expression in wild-type and -null mice at postnatal day 21 (P21) following and lactational exposure. The results showed that TCDD preferentially induced the AHR target genes and in the lower infundibulum and subjacent junctional zone overlapping the LRIG1+ progenitor cell niche. TCDD also caused -dependent seboatrophy, accompanied by increased expression of , a transcriptional repressor that regulates SG size. A second site of induction was the SG, where was markedly elevated in the basal proliferating cells and immature sebocytes. In a 3-day topical exposure study of early effects, TCDD produced a dose-dependent increase of expression in the SG that included the more differentiated sebocytes. This response was accompanied by expansion of the -positive area, elevated Nile Red lipid staining, and an increased number of -high sebocytes, demonstrating that TCDD enhanced SG differentiation and lipid production . These changes preceded the onset of -dependent seboatrophy, providing new insight into the cellular and molecular events underlying chloracne pathogenesis. - Source: PubMed
Publication date: 2026/07/23
Tasnim Syeda MashniaSolanki SubhashBhuju JyotiThompson LaurenSkalli OmarGrice Elizabeth ASutter Carrie HayesSutter Thomas R - To investigate the role of Notch1 signaling in Lrig1-expressing vocal fold (VF) epithelial stem cells during epithelial repair following acute injury. - Source: PubMed
Publication date: 2026/07/15
Cai JieThibeault Susan LLungova Vlasta - Fasting enhances small intestinal regeneration after radiation, but the contribution of the gut microbiome to this process remains uncharacterized. We identify () as a key mediator of this response. was enriched in fasted mice and its antibiotic depletion abrogated radioprotection, whereas reintroduction restored both organismal survival and intestinal integrity. Fasting elevated propionic acid, consistent with 's metabolic output. -conditioned medium and propionate induced histone H3 acetylation in intestinal stem cell cultures while in vivo fasting induced -dependent H3K27ac and H3K9ac, remodeling promoter-enhancer landscapes in crypt epithelial cells. Epigenetic profiling revealed a rewired core regulatory program enriched for pioneer transcription factors (Foxa, Gata, Klf), architectural organizers (Ctcf, Boris), and lineage-defining and metabolic regulators (Cdx2, Hnf4). This program supports expansion of a population of primed persister cells characterized by open chromatin accessibility at key stem and regenerative-associated loci including , , These findings define a fasting-induced microbiome-metabolite-chromatin axis that epigenetically primes highly plastic persister cells for rapid regeneration of the intestinal epithelium following radiation-induced injury. - Source: PubMed
Publication date: 2026/06/23
Barrodia PraveenSaw Ajay KumarJeter-Jones Sabrina LChang Chia-ChiShao JiansuArslan EmreSingh Anand KSatpati SureshJenq Robert RRai KunalPiwnica-Worms Helen