Recombinant Human SIGLEC6 /CD327 Protein
- Known as:
- Recombinant Human SIGLEC6 /CD327 Protein
- Catalog number:
- si-796
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human SIGLEC6 /CD327 Protein
Related genes to: Recombinant Human SIGLEC6 /CD327 Protein
- Gene:
- SIGLEC6 NIH gene
- Name:
- sialic acid binding Ig like lectin 6
- Previous symbol:
- CD33L, CD33L1
- Synonyms:
- OB-BP1, SIGLEC-6, CD327
- Chromosome:
- 19q13.41
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-17
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human SIGLEC6 /CD327 Protein
Related articles to: Recombinant Human SIGLEC6 /CD327 Protein
- Mast cell elimination through Siglec-6 is a minimally explored strategy for diseases characterized by mast cell overactivity or overproduction. - Source: PubMed
Publication date: 2026/06/29
Thames Ariel HelmsRische Clayton HKrier-Burris Rebecca ACao YunHunt Andrew CKlug NatalieZelenetz Stephanie RBurleigh Evan RAw RochelleWong Derek AShaver Zachary MSeki KosukeGuerrero LauraFernandez ReginaSharma SwagatBochner Bruce SJewett Michael CScott Evan AO'Sullivan Jeremy A - Acute myeloid leukemia (AML) remains a highly aggressive malignancy with limited therapeutic options and poor long-term survival. A major barrier to curative treatment is the persistence of leukemic stem cells (LSCs), a chemo-resistant population that drives relapse. Chimeric antigen receptor (CAR)-T-cell therapy has transformed the treatment of B-cell hematological malignancies. However, its application in AML has been met with significant challenges. Among the key challenges are the scarcity of AML-specific antigens and the risk of on-target/off-tumor toxicity due to shared antigen expression on normal hematopoietic stem cells (HSCs) and/or mature blood cells. Early clinical trials of CAR-T-cell therapy in AML -primarily targeting CD123, CD33, or CLL‑1- have demonstrated limited durable complete remissions and/or frequent myeloablation, underscoring the need for more selective targets. While other targets show more restricted expression profiles, they are often expressed only in a small subgroup of AML patients. In this review, we systematically evaluated 63 AML-associated antigens for which CAR constructs have been reported, using five criteria: (1) homogeneous expression across AML patients, (2) uniform expression on AML cells within individual patients; (3) presence on LSCs, (4) absence on normal HSCs, and (5) no or acceptable expression on mature blood cells. Applying a 20-point scoring framework, 13 novel antigens emerged as the most promising candidates for CAR-T-cell therapy in AML: ADGRE2, SIGLEC-6, IL1RAP, MUC1, CCR1, CD155, CD70, LILRB4, GRP78, CD37, ITGB2, TIM-3 and mesothelin. We discuss the advantages and limitations of each target, along with strategies to mitigate associated risks. With no CAR-T-cell therapy currently approved for AML, this comprehensive review provides a prioritized antigen landscape and a framework to guide the rational design of next-generation CARs for this challenging malignancy. - Source: PubMed
Publication date: 2026/06/20
Van Oers FlorianFlumens DonovanHaentjens SimonKrekelbergh LaurensAnguille Sébastien - Early-onset preeclampsia (EO-PE) is a severe pregnancy complication driven by defective trophoblast syncytialization and an exacerbated inflammatory microenvironment. Although Sialic acid-binding immunoglobulin-like lectin 6 (SIGLEC6) is implicated in PE, its precise cellular localization, functional impact on trophoblast-immune crosstalk, and the underlying molecular signaling driving these pathologies remain largely uncharacterized. - Source: PubMed
Publication date: 2026/06/01
Tong XinyueZhao RanLi MinXu YimingYang YuqiZhou BaochengHuang FengWang Mei - Chronic urticaria (CU) is a skin disease characterized by recurrent episodes of vascular dilation and increased permeability of the cutaneous and mucosal microvasculature. Although antihistamines and omalizumab remain first-line and second-line therapies, respectively, a significant proportion of patients develop recalcitrant disease phenotypes, highlighting critical unmet needs for innovative therapeutic paradigms. In recent years, emerging insights into Mas-related G protein-coupled receptor X2 (MRGPRX2) have revealed transformative perspectives for elucidating the pathobiology of refractory CU. As a class A G protein-coupled receptor (GPCR) that is predominantly localized to mast cells, MRGPRX2 orchestrates non-IgE-mediated mast cell degranulation through its pluripotent ligand recognition capacity, engaging diverse exogenous cationic compounds, neuropeptides, and certain pharmacological agents. This comprehensive review evaluates recent advancements in deciphering the mechanistic contributions of MRGPRX2 to CU pathogenesis, with the ultimate aim of informing the development of precision diagnostic and therapeutic frameworks for CU management. - Source: PubMed
Publication date: 2026/04/23
Wu KunLiu Junlin - BACKGROUND: Relapsed/refractory pediatric acute myeloid leukemia (AML) remains a significant therapeutic challenge, largely due to the persistence of leukemia stem cells (LSCs), antigen heterogeneity and off-tumor toxicity. Siglec6 and CD37 are highly expressed in AML LSC subpopulations. To enhance specificity and reduce relapse risk, we explored the efficacy of a bispecific CD37–Siglec6 chimeric antigen receptor (CAR) T-cell strategy, where both receptors are enriched on AML LSCs. METHODS: Single-cell RNA sequencing data from the GEO dataset and Bulk RNA-sequencing were subsequently obtained from newly diagnosed, remission, and relapsed patients’ AML bone marrow samples. Meanwhile, Siglec6 CAR, CD37 CAR, and CD37–Siglec6 bispecific CAR constructs were prepared. CAR genes were synthesized and cloned into lentiviral vectors, which were then packaged in 293T cells. Lentivirus was transduced to generate Siglec6 CAR-T, CD37 CAR-T, and CD37–Siglec6 CAR-T cells. In vitro assays were used to assess CAR expression, immunophenotype, cytotoxicity against U-937 cells, and cytokine secretion. In vivo efficacy was evaluated in an NSG mouse model engrafted with luciferase‑U-937 cells. RESULTS: Siglec6 was highly expressed in erythroid progenitors and malignant blasts, which was correlated with relapse and showed potential interaction with CD37 via protein‑network analysis. Compared with single‑target CAR constructs, the bispecific CD37–Siglec6 CAR‑T cells exhibited higher transduction efficiency (52.8%) and expansion (145‑fold). Furthermore, these bispecific CAR-T cells displayed an enriched central and effector memory phenotype, reduced TIM‑3 expression, and superior cytotoxicity in vitro (87.8% specific killing at 48 h), accompanied by elevated IFN‑γ, TNF‑α and IL‑6 secretion. In vivo, CD37‑Siglec6 CAR‑T cells achieved the most potent tumor control, prolonged median survival (60 days), and they demonstrated enhanced persistence in the bone marrow, spleen and peripheral blood, while showing few signs of acute toxicity. CONCLUSION: Bispecific CD37–Siglec6 CAR‑T cells exhibit enhanced anti‑AML activity, improved persistence, and a favorable safety profile in preclinical models. Importantly, these bispecific CD37–Siglec6 CAR-T cells demonstrated enhanced preclinical efficacy against AML cell lines without significantly affecting normal hematopoiesis, providing a promising therapeutic strategy for pediatric AML. - Source: PubMed
Publication date: 2026/04/25
Wang LipingWang YufeiWang XinyeDai YuanyuanDeng YanbingHuang TiantuoWen ChaoJin XiaoliTong ShoufangSun WeiyueWeng Wenwen