EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #01700_C
用于鉴定、评估和分离表达高水平ALDH的干细胞和祖细胞
若您需要咨询产品或有任何技术问题，请通过官方电话 400 885 9050 或邮箱 info.cn@stemcell.com 与我们联系。
New look, same high quality and support! You may notice that your instrument or reagent packaging looks slightly different from images displayed on the website, or from previous orders. We are updating our look but rest assured, the products themselves and how you should use them have not changed. Learn more
总览
用ALDEFLUOR™试剂盒鉴定和分离表达醛脱氢酶（ALDH）的活细胞。与传统方法相比，该检测方法不需要抗体染色。已有研究报道，不同谱系的正常和癌症前体细胞中普遍存在高水平 ALDH 表达。ALDEFLUOR™检测是一种被广泛发表的用于检测ALDH 高表达（ALDHbr）细胞的非免疫学方法，可用于检测造血、乳腺、内皮、间充质、神经和其他组织中的癌细胞。试剂盒中包含的ALDEFLUOR™DEAB试剂和ALDEFLUOR™ 检测缓冲液支持检测的最佳效果，二者也可单独购买。该试剂盒与标准流式细胞仪兼容，可用于 ALDHbr 细胞的后续分析，并与标准细胞分选仪兼容，可用于进一步纯化和表征。查看我们的其他资源，以了解更多关于ALDEFLUOR™试剂系统的信息。
细胞类型
脑肿瘤干细胞，癌细胞及细胞系，造血干/祖细胞，乳腺细胞，间充质干/祖细胞，神经干/祖细胞，其他物种
种属
人，小鼠，非人灵长类，其他物种，大鼠
应用
流式细胞术
品牌
ALDEFLUOR
研究领域
癌症，上皮细胞研究，神经科学，干细胞生物学
CAS 编号
7647-01-0
实验数据
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
应用领域
本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。
相关材料与文献
技术资料 (23)
常见问题 (21)
文献 (302)
The PCNA inhibitor AOH1996 suppresses cancer stemness and enhances anti-PD1 immunotherapy in squamous cell carcinoma
Stem Cell Research & Therapy 2025 Sep
Abstract
Proliferating cell nuclear antigen (PCNA), a well-documented anticancer target, is critical for DNA synthesis, replication, and repair. AOH1996, a small-molecule PCNA inhibitor, is currently undergoing clinical trials for the treatment of advanced solid tumors. However, the therapeutic effect of AOH1996 on head and neck squamous cell carcinoma (HNSCC) remains unclear. The effects of AOH1996 on HNSCC biological behaviors and cancer stemness were tested in HNSCC cells and nude mice. The combination treatment of AOH1996 and anti-PD1 was performed in a 4-nitroquinoline N-oxide (4NQO)-induced HNSCC mouse model. RNA sequencing, Western Blotting, immunofluorescence staining, comet assays, and qRT‒PCR were conducted for mechanistic studies. Our results showed that AOH1996 effectively inhibited HNSCC proliferation and invasion both in vitro and in vivo. AOH1996 suppressed HNSCC stemness, development, and metastasis. Moreover, AOH1996 altered the tumor immune microenvironment into an inflamed state with increased CD8 + T-cell infiltration, rendering it a favorable partner for combination therapy with immune checkpoint inhibitors. Mechanistically, AOH1996 induced cellular DNA damage, suppressed cancer stemness through the upregulation of p-TBK1, and promoted the secretion of CD8 + T-cell-recruiting chemokines by stimulating IRF3-mediated transcription. Taken together, our results demonstrated that AOH1996 suppressed tumor growth, eliminated cancer stem cells (CSCs), and synergistically enhanced the efficacy of anti-PD1 immunotherapy in HNSCC. The online version contains supplementary material available at 10.1186/s13287-025-04607-9.
BNIP3L/BNIP3‐Mediated Mitophagy Contributes to the Maintenance of Ovarian Cancer Stem Cells
Journal of Cellular and Molecular Medicine 2025 Oct
Abstract
Ovarian cancer remains the most lethal gynaecological malignancy, with tumour recurrence and chemoresistance posing significant therapeutic challenges. Emerging evidence suggests that cancer stem cells (CSCs), a rare subpopulation within tumours with self‐renewal and differentiation capacities, contribute to these hurdles. Therefore, elucidating the mechanisms that sustain CSCs is critical for improving treatment strategies. Mitophagy, a selective process for eliminating damaged mitochondria, plays a key role in maintaining cellular homeostasis, including CSC survival. Our study demonstrates that ovarian CSCs exhibit enhanced mitophagy, accompanied by elevated expression of the mitochondrial outer membrane receptors BNIP3 and BNIP3L. Knockdown of BNIP3 or BNIP3L significantly reduces mitophagy and impairs CSC self‐renewal, indicating that receptor‐mediated mitophagy is essential for CSC maintenance. Mechanistically, we identify that hyperactivated NF‐κB signalling drives the upregulation of BNIP3 and BNIP3L in ovarian CSCs. Inhibition of NF‐κB signalling, either via p65 knockdown or pharmacological inhibitors, effectively suppresses mitophagy. Furthermore, we demonstrate that elevated DNA‐PK expression contributes to the constitutive activation of NF‐κB signalling, thereby promoting mitophagy in ovarian CSCs. In summary, our findings establish that BNIP3/BNIP3L‐mediated mitophagy, driven by DNA‐PK‐dependent NF‐κB hyperactivation, is essential for CSC maintenance. Targeting the DNA‐PK/NF‐κB/BNIP3L‐BNIP3 axis to disrupt mitochondrial quality control in CSCs represents a promising therapeutic strategy to prevent ovarian cancer recurrence and metastasis.
YTHDC2 suppresses bladder cancer by inhibiting SOX2-mediated tumor plasticity
Cell Death & Disease 2025 Oct
Abstract
Pluripotent cancer stem cells play a pivotal role in inducing phenotypic plasticity across various cancer types, including bladder cancer. This plasticity, crucial for cancer progression, is largely regulated by epigenetic modifications including N6-methyladenosine (m6A) in RNAs. However, the role of the m6A reader protein YTHDC2 in this process remains poorly understood. In this study, we uncovered that the depletion of YTHDC2 significantly increased the pool of bladder cancer stem cells (BCSCs), resulting in a phenotypic shift towards a more invasive subtype of bladder cancer. This shift was characterized by enhanced proliferation, migration, invasion, and self-renewal capabilities of cancer cells, highlighting YTHDC2’s function as a tumor suppressor. Mechanistically, YTHDC2 recognized and bound to m6A-modified SOX2 mRNA, resulting in translational inhibition of SOX2. In conclusion, our study identifies YTHDC2 as a tumor suppressor in bladder cancer through inhibiting SOX2-mediated cell pluripotency and underscores the therapeutic potential of targeting the YTHDC2-SOX2 axis in bladder cancer.
相关材料与文献
技术资料 (23)
常见问题 (21)
文献 (302)
The PCNA inhibitor AOH1996 suppresses cancer stemness and enhances anti-PD1 immunotherapy in squamous cell carcinoma
Stem Cell Research & Therapy 2025 Sep
Abstract
Proliferating cell nuclear antigen (PCNA), a well-documented anticancer target, is critical for DNA synthesis, replication, and repair. AOH1996, a small-molecule PCNA inhibitor, is currently undergoing clinical trials for the treatment of advanced solid tumors. However, the therapeutic effect of AOH1996 on head and neck squamous cell carcinoma (HNSCC) remains unclear. The effects of AOH1996 on HNSCC biological behaviors and cancer stemness were tested in HNSCC cells and nude mice. The combination treatment of AOH1996 and anti-PD1 was performed in a 4-nitroquinoline N-oxide (4NQO)-induced HNSCC mouse model. RNA sequencing, Western Blotting, immunofluorescence staining, comet assays, and qRT‒PCR were conducted for mechanistic studies. Our results showed that AOH1996 effectively inhibited HNSCC proliferation and invasion both in vitro and in vivo. AOH1996 suppressed HNSCC stemness, development, and metastasis. Moreover, AOH1996 altered the tumor immune microenvironment into an inflamed state with increased CD8 + T-cell infiltration, rendering it a favorable partner for combination therapy with immune checkpoint inhibitors. Mechanistically, AOH1996 induced cellular DNA damage, suppressed cancer stemness through the upregulation of p-TBK1, and promoted the secretion of CD8 + T-cell-recruiting chemokines by stimulating IRF3-mediated transcription. Taken together, our results demonstrated that AOH1996 suppressed tumor growth, eliminated cancer stem cells (CSCs), and synergistically enhanced the efficacy of anti-PD1 immunotherapy in HNSCC. The online version contains supplementary material available at 10.1186/s13287-025-04607-9.
BNIP3L/BNIP3‐Mediated Mitophagy Contributes to the Maintenance of Ovarian Cancer Stem Cells
Journal of Cellular and Molecular Medicine 2025 Oct
Abstract
Ovarian cancer remains the most lethal gynaecological malignancy, with tumour recurrence and chemoresistance posing significant therapeutic challenges. Emerging evidence suggests that cancer stem cells (CSCs), a rare subpopulation within tumours with self‐renewal and differentiation capacities, contribute to these hurdles. Therefore, elucidating the mechanisms that sustain CSCs is critical for improving treatment strategies. Mitophagy, a selective process for eliminating damaged mitochondria, plays a key role in maintaining cellular homeostasis, including CSC survival. Our study demonstrates that ovarian CSCs exhibit enhanced mitophagy, accompanied by elevated expression of the mitochondrial outer membrane receptors BNIP3 and BNIP3L. Knockdown of BNIP3 or BNIP3L significantly reduces mitophagy and impairs CSC self‐renewal, indicating that receptor‐mediated mitophagy is essential for CSC maintenance. Mechanistically, we identify that hyperactivated NF‐κB signalling drives the upregulation of BNIP3 and BNIP3L in ovarian CSCs. Inhibition of NF‐κB signalling, either via p65 knockdown or pharmacological inhibitors, effectively suppresses mitophagy. Furthermore, we demonstrate that elevated DNA‐PK expression contributes to the constitutive activation of NF‐κB signalling, thereby promoting mitophagy in ovarian CSCs. In summary, our findings establish that BNIP3/BNIP3L‐mediated mitophagy, driven by DNA‐PK‐dependent NF‐κB hyperactivation, is essential for CSC maintenance. Targeting the DNA‐PK/NF‐κB/BNIP3L‐BNIP3 axis to disrupt mitochondrial quality control in CSCs represents a promising therapeutic strategy to prevent ovarian cancer recurrence and metastasis.
YTHDC2 suppresses bladder cancer by inhibiting SOX2-mediated tumor plasticity
Cell Death & Disease 2025 Oct
Abstract
Pluripotent cancer stem cells play a pivotal role in inducing phenotypic plasticity across various cancer types, including bladder cancer. This plasticity, crucial for cancer progression, is largely regulated by epigenetic modifications including N6-methyladenosine (m6A) in RNAs. However, the role of the m6A reader protein YTHDC2 in this process remains poorly understood. In this study, we uncovered that the depletion of YTHDC2 significantly increased the pool of bladder cancer stem cells (BCSCs), resulting in a phenotypic shift towards a more invasive subtype of bladder cancer. This shift was characterized by enhanced proliferation, migration, invasion, and self-renewal capabilities of cancer cells, highlighting YTHDC2’s function as a tumor suppressor. Mechanistically, YTHDC2 recognized and bound to m6A-modified SOX2 mRNA, resulting in translational inhibition of SOX2. In conclusion, our study identifies YTHDC2 as a tumor suppressor in bladder cancer through inhibiting SOX2-mediated cell pluripotency and underscores the therapeutic potential of targeting the YTHDC2-SOX2 axis in bladder cancer.
更多信息
| 物种 | 人类, 其它物种, 大鼠, 小鼠, 非人灵长类 |
|---|---|
| Cas Number | 7647-01-0 |
相关产品
-
ALDEFLUOR™测定缓冲液用于ALDEFLUOR™试剂盒的附加检测缓冲液
-
ALDEFLUOR™DEAB试剂在ALDEFLUOR™检测系统中用作对照的ALDH酶抑制剂
-
MammoCult™ 人源培养基套装用于人乳腺球和肿瘤球的培养
-
抗人CD34抗体，clone 581小鼠Monoclonal IgG1抗体，抗人CD34
法律声明:
ALDEFLUOR is registered trademark of ALDAGEN Inc. 质量保证:
产品仅供研究使用，不用于针对人或动物的诊断或治疗。 欲获悉更多关于STEMCELL的质控信息，请访问 STEMCELL.CN/COMPLIANCE.
ALDEFLUOR is registered trademark of ALDAGEN Inc. 质量保证:
产品仅供研究使用，不用于针对人或动物的诊断或治疗。 欲获悉更多关于STEMCELL的质控信息，请访问 STEMCELL.CN/COMPLIANCE.
沪公网安备31010102008431号
在线联系