LRRC15 antibody (FITC)
- Known as:
- LRRC15 (anti-) (fluorecein)
- Catalog number:
- orb102931
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- LRRC15 antibody (FITC)
Related genes to: LRRC15 antibody (FITC)
- Gene:
- LRRC15 NIH gene
- Name:
- leucine rich repeat containing 15
- Previous symbol:
- -
- Synonyms:
- LIB
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-25
- Date modifiied:
- 2015-08-27
Related products to: LRRC15 antibody (FITC)
Related articles to: LRRC15 antibody (FITC)
- Leucine-rich-repeat-containing protein 15 (LRRC15) is selectively expressed on cancer-associated fibroblasts (CAFs) and constitutes a promising biomarker for imaging the tumor microenvironment. Using a combinatorial library approach, assisted by machine learning, we developed disulfide-constrained peptides (DCPs), notably ML-YSD-07 and ML-PD-03, that demonstrate subnanomolar affinities for murine LRRC15 (muLRRC15) and specifically localize onto muLRRC15-expressing fibroblasts. PET imaging with F-radiolabeled ML-YSD-07 exhibits specific tumor accumulation in a murine pancreatic cancer model highly enriched with LRRC15-expressing CAFs. Crystal structures of apo-muLRRC15 and of ML-YSD-07-bound muLRRC15 show that the DCPs evolved to adopt a distinct binding conformation that efficiently interacts with a flat epitope on muLRRC15. Collectively, this work identifies potent, molecularly engineered LRRC15-binding peptides and further highlights LRRC15 as a valuable CAF biomarker for cancer imaging applications. - Source: PubMed
Publication date: 2026/06/05
Tombling Benjamin JCai FeiWendorff Timothy JOgasawara AnnieGill Herman STinianow Jeff NChang AndrewBalana Aaron TPeng LinglingMiller Stephen EWalters Benjamin TLictao AaronYu QinyingDeWitt David CWei YuehuaWu Sunny ZSudhamsu JawaharKrishnamurty Akshay TWilliams Simon PMarik JanZhang YingnanMaun Henry RKirchhofer Daniel - Taenia solium (T. solium) and its larval infections cause cysticercosis and taeniasis, posing serious threats to human health and livestock industry development. Our research group has, for the first time, successfully identified a leucine-rich repeat-containing protein 15 (LRRC15) from the (excretory secretory antigens, ESAs) of T. solium and demonstrated its ability to regulate the differentiation of host regulatory T cells (Tregs). This protein may be a critical factor in the pathogenicity of T. solium and its larvae. Our findings reveal that LRRC15 induces an immune differentiation between Tregs and T helper type 17 cells (Th17), and the underlying molecular mechanisms remain unreported. Through transcriptomic analysis, we identified the PI3K/Akt/mTORC1 signaling pathway, which is associated with Treg and Th17 cell differentiation. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot were employed to validate key targets and critical factors within this signaling pathway. This study aims to provide a scientific foundation for elucidating the immune pathogenic mechanisms of cysticercosis. - Source: PubMed
Publication date: 2026/06/03
Yu ShunfuSun XiaoqingMu QianqianZhou BiyingLiu Meichen - Pancreatic intraepithelial neoplasia (PanIN) precedes pancreatic cancer, a deadly disease characterized by an extensive tumor microenvironment. How the microenvironment evolves during cancer progression is largely unknown, as PanINs are microscopic and non-diseased pancreas samples are exceedingly rare, while adjacent normal samples are disrupted by the presence of malignancy. Leveraging donor organs and spatial technologies we mapped the evolution of PanIN to cancer. The PanIN epithelial component falls on a continuum with cancer while the PanIN microenvironment is drastically distinct. Progression to cancer is accompanied by profound geographical reorganization of myeloid cells and lymphocytes and the formation of a cancer-specific fibroblast population characterized by high levels of Smooth Muscle Actin, LRRC15 and the WNT signaling component LEF1. Together, our data show asynchronous evolution of epithelial and stromal components during pancreatic carcinogenesis. Lack of stromal reprogramming might explain why most PanINs do not progress to cancer. Compiled data available at https://pascadimagliano-lab.github.io/PancAtlas. - Source: PubMed
Publication date: 2026/05/21
Elhossiny Ahmed MKadiyala PadmaOkoye Jude OgechukwuHiraki Harrison LProcario Megan CGiridharan ThejaswiniWatkoske Hannah RTannus Ruckert MarianaWang JiayueGriffith Brian DBray Alexander WMills Jamie NEspinoza Carlos EZeller JörgPeterson NicoleBednar FilipZhang YaqingRao ArvindLyssiotis Costas ASzczepanski Julianne MShi JiaqiDeshpande AtulMaitra AnirbanFertig Elana JCarpenter Eileen SFrankel Timothy LPasca di Magliano Marina - Fibroblasts are key potentiators of chronic disease pathophysiology. Despite their established roles in promoting pathological inflammation and tissue remodeling, activated myofibroblasts are generally characterized as a single, homogeneous cell population, obscuring critical functional distinctions. Defining the cell states, their molecular regulators, and restricted markers is critical to developing effective therapies for the treatment of fibrosis. Here, using a human lung stromal cell atlas of idiopathic pulmonary fibrosis, we identify two myofibroblast transcriptional states associated with distinct predicted biological function, regulation, and cell surface marker expression. We identify fibroblast-specific TGFb signaling as the key regulator of the mechanistic switch from a wound healing-associated and proliferative to a profibrotic myofibroblast. Further, we elucidate conserved TGFb-dependent and suppressed gene expression programs that define these states. Our findings reveal that LRRC15 is highly restricted to myofibroblasts that primarily express an extracellular matrix-remodeling gene program and illuminate that this key cell state can differentiate in the absence of an obligate inflammatory precursor intermediate. Last, we apply machine learning using a human single-cell foundation model to demonstrate broad applicability of the biology described herein to human chronic disease. - Source: PubMed
Publication date: 2026/05/20
Shyer Justin AWehbe FabienDavidson Christopher DBender Hannah SThai MinhCox ChristianMissarova AlsuArlantico AlexanderHall BenZhang RuoyuKim DavidAltieri AnthonyHasan ShakirNamdar AfshinChen TinaHakim Shaheed WGuidos CynthiaBrightbill Hans DKuo TonyHeimberg GrahamCorrada Bravo HéctorRatsimandresy Rojo AUttarwar SalilTeng GraceSalem OmarArjomandi MehrdadWilson Mark SDarmanis SpyrosZiai JamesScherl AlexisModrusan ZoraWolters Paul JBuechler Matthew BVander Heiden Jason ATurley Shannon J - Pancreatic ductal adenocarcinoma (PDAC) is characterized by a highly immunosuppressive and desmoplastic tumor microenvironment (TME) that limits the efficacy of immunotherapy. However, the evolution of this immunosuppressive TME and the underlying mechanisms remain incompletely understood. Here, we construct a dynamic single-cell atlas spanning uninvolved adjacent pancreatic tissue (UNIN), intraductal papillary mucinous neoplasm (IPMN), and PDAC. We confirm the stepwise establishment of an immunosuppressive milieu, accompanied by the emergence of LRRC15 fibroblasts as determinants. Functional assays further identify tumor-derived LAMB3 as a regulator of LRRC15 fibroblast differentiation. Mechanistically, LAMB3 promotes FOSL2-dependent transcriptional activation of LRRC15 through the ITGB1/FAK/MAPK signaling axis, ultimately suppressing T cell cytotoxicity. Orthotopic models reveal that LAMB3 overexpression increases the LRRC15 positive area and impairs T cell cytotoxicity, whereas FAK inhibition partially reverses these effects. In parallel, LAMB3 knockdown reduces the LRRC15 positive area and improves the efficacy of PD-1 blockade. Moreover, glycolytic reprogramming in PDAC ductal cells upregulates LAMB3 expression and correlates with increased LRRC15 fibroblast enrichment. Clinically, co-enrichment of LAMB3 PDAC ductal cells and LRRC15 fibroblasts is associated with inferior overall survival. Collectively, our findings define a dynamic ductal-fibroblast-immune multicellular axis underlying PDAC pathogenesis and provide insights into potential therapeutic strategies. - Source: PubMed
Publication date: 2026/05/19
Shi XuqingLiu HangqiSun JianruLiu XiaodingJv XinpingChen LongyunZhang YuhanZhang HuiXing XudongLi RuiyuKe XinyiWang JunYin XianglinLiu BohanLiu QixianWang YuanLu JunliangLiu ShiyiPang JunyiCai YumengDai MenghuaBai FanWu HuanwenLiang Zhiyong