识别病原体相关分子模式或损伤相关分子模式的免疫受体，能激活先天免疫应答，启动炎症反应和适应性免疫。
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| 产品号 | 产品名称 | 蛋白编码 | 图片 |
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| ALP6690 | Q2HZ94 (L19-A1388) |
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| CD206/MMR 蛋白在巨噬细胞中充当多功能介质，促进糖蛋白内化。它具有广泛的结合能力，可与硫酸化和非硫酸化多糖链相互作用。 | |||
| ALP6574 | D3ZPN6 (V30-K190) |
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| CLEC5A/MDL-1 蛋白正向调节破骨细胞生成并调节炎症反应。它作为登革热病毒血清型 1-4 的关键巨噬细胞受体，通过 TYROBP 磷酸化触发信号传导。这种相互作用刺激促炎细胞因子的释放，而无需病毒进入。 | |||
| ALP8115 | Q8WTT0-1(Phe46-Ile213) |
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| The 4-1BBL is the high affinity ligand of 4-1BB, also known as CD137L or TNFSF9. 4-1BB ligand (4-1BBL) is an inducible molecule present on several APC types, including B cells, macrophages and DCs.4-1BB:4-1BBL pathway seems to amplify the existing costimulatory signals, even if the engagement of 4-1BB in the presence of a strong TCR signaling can induce IL-2 production in a CD28-independent manner. | |||
| ALP8116 | Q8WTT0-1(Phe46-Ile213) |
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| BDCA-2, BDCA-3, and BDCA-4. In blood, BDCA-2 and BDCA-4 are expressed on CD11c(-) CD123(bright) plasmacytoid dendritic cells, whereas BDCA-3 is expressed on small population of CD11c() CD123(-) dendritic cells. All three Ags are not detectable on a third blood dendritic cell population, which is CD1c() CD11c(bright) CD123(dim), or on any other cells in blood.BDCA-2 is completely down-regulated on plasmacytoid CD11c(-) CD123(bright) dendritic cells, BDCA-2 is rapidly internalized at 37 degrees C after mAb labeling. | |||
| ALP8183 | Q12918-1(Gln67-Ser225) |
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| CD161 (NKRP1) is a lectin-like receptor present on NK cells and rare T-cell subsets. We have observed CD161 expression in some cases of T-cell prolymphocytic leukemia (T-PLL) and found it to be useful in follow-up and detection of disease after treatment. | |||
| ALP8186 | Q12918-1(Gln67-Ser225) |
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| CD161 (NKRP1) is a lectin-like receptor present on NK cells and rare T-cell subsets. We have observed CD161 expression in some cases of T-cell prolymphocytic leukemia (T-PLL) and found it to be useful in follow-up and detection of disease after treatment. | |||
| ALP8198 | P27811(Gln67-His227) |
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| CD161 (NKRP1) is a lectin-like receptor present on NK cells and rare T-cell subsets. We have observed CD161 expression in some cases of T-cell prolymphocytic leukemia (T-PLL) and found it to be useful in follow-up and detection of disease after treatment. | |||
| ALP8335 | Q9UHP7-1(Arg60-Val191) |
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| C-type lectin domain family 2, member D (CLEC2D) is implicated in the immune response. Pre-eclampsia and HIV infection have opposing immune responses. The contrasting expression of CLEC2D in HIV infection and pre-eclampsia is demonstrative of the immunosuppressive and pro-inflammatory roles of the respective pathologies. However, this implication may be confounded by highly active anti-retroviral treatment (HAART). | |||
| ALP8338 | Q8IUN9-2(Gln61-His292) |
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| CLEC10A, (C-type lectin domain family 10, member A), as the member of C-type lectin receptors (CLRs), plays a vital role in modulating innate immunity and adaptive immunity and has shown great potential as an immunotherapy target for cancers. However, there is no functional research of CLEC10A in prognostic risk, immunotherapy or any other treatment of lung adenocarcinoma (LUAD). | |||
| ALP8337 |
Recombinant Cynomolgus CLEC12A/MICL/CLL-1 Protein,Cynomolgus,N-His,Expi293 重组蛋白Cynomolgus CLEC12A/MICL/CLL-1 Protein,Cynomolgus,N-His,Expi293 |
A0A2K5WXQ6(His32-Ala232) |
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| CLEC12A has recently been identified as an antigen, expressed on leukemic stem cells and leukemic blasts. Given the fact that this expression profile seems stable throughout diagnosis, treatment and relapse on leukemic blasts and leukemic stem cells, CLEC12A can be considered a highly potent and reliable marker for the detection of measurable residual disease and therefore applicable for risk stratification and prognostication in AML. | |||
| ALP8346 | Q9R007-1(Tyr26-Lys190) |
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| In C. elegans, increased lifespan in daf-2 insulin/IGF-1 receptor mutants is accompanied by up-regulation of the MDL-1 Mad basic helix-loop-helix leucine zipper transcription factor.MDL-1, like its mammalian orthologs, is an inhibitor of cell proliferation and growth that slows progression of an age-related pathology in C. elegans (uterine tumors). In addition, intestine-limited rescue of mdl-1 increased lifespan but not to wild type levels. Thus, mdl-1 likely acts both in the intestine and the germline to influence age-related mortality. | |||
| ALP8339 |
Recombinant Human CLEC12A/MICL/CLL-1 Protein,Human,N-His,Expi293 |
Q5QGZ9-2(His65-Ala265) |
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| CLEC12A has recently been identified as an antigen, expressed on leukemic stem cells and leukemic blasts. Given the fact that this expression profile seems stable throughout diagnosis, treatment and relapse on leukemic blasts and leukemic stem cells, CLEC12A can be considered a highly potent and reliable marker for the detection of measurable residual disease and therefore applicable for risk stratification and prognostication in AML. | |||
| ALP8345 |
Recombinant Mouse CLEC12A/MICL/CLL-1 Protein,Mouse,N-His,Expi293 |
Q504P2-1(Tyr65-Arg267) |
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| CLEC12A has recently been identified as an antigen, expressed on leukemic stem cells and leukemic blasts. Given the fact that this expression profile seems stable throughout diagnosis, treatment and relapse on leukemic blasts and leukemic stem cells, CLEC12A can be considered a highly potent and reliable marker for the detection of measurable residual disease and therefore applicable for risk stratification and prognostication in AML. | |||
| ALP8340 |
Recombinant Human CLEC12A/MICL/CLL-1 Protein,Human,N-hFc,Expi293 |
Q5QGZ9-2(His65-Ala265) |
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| CLEC12A has recently been identified as an antigen, expressed on leukemic stem cells and leukemic blasts. Given the fact that this expression profile seems stable throughout diagnosis, treatment and relapse on leukemic blasts and leukemic stem cells, CLEC12A can be considered a highly potent and reliable marker for the detection of measurable residual disease and therefore applicable for risk stratification and prognostication in AML. | |||
| ALP8341 | Q9NY25-1(Tyr26-Lys188) |
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| In C. elegans, increased lifespan in daf-2 insulin/IGF-1 receptor mutants is accompanied by up-regulation of the MDL-1 Mad basic helix-loop-helix leucine zipper transcription factor.MDL-1, like its mammalian orthologs, is an inhibitor of cell proliferation and growth that slows progression of an age-related pathology in C. elegans (uterine tumors). In addition, intestine-limited rescue of mdl-1 increased lifespan but not to wild type levels. Thus, mdl-1 likely acts both in the intestine and the germline to influence age-related mortality. | |||
| ALP8342 | Q6UXN8(Lys57-Val241) |
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| CLEC9A expression was significantly higher in psoriatic skin compared with healthy donor. In psoriatic skin and PsA ST, CLEC9A() cells were in close proximity to TUNEL() cells. SF CLEC9A levels were significantly lower compared with paired PsA serum. Adalimumab treatment did not affect CLEC9A serum level and skin expression. The downregulation of synovial CLEC9A might be associated with a novel mechanism by which anti-TNF therapy might reduce CD8-mediated inflammation in PsA patients. | |||
| ALP9062 | Q6PCD4(Ser23-Glu703) |
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| TLR3 is expressed in the central nervous system (CNS), where it is required to control HSV-1, which spreads from the epithelium to the CNS via cranial nerves. TLR3 is also expressed in epithelial and dendritic cells, which apparently use TLR3-independent pathways to prevent further dissemination of HSV-1 and to provide resistance to other pathogens in TLR3-deficient patients. Human TLR3 appears to be redundant in host defense to most microbes but is vital for natural immunity to HSV-1 in the CNS, which suggests that neurotropic viruses have contributed to the evolutionary maintenance of TLR3. | |||
| ALP9063 | Q99MB1(Thr25-Leu705) |
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| TLR3 is expressed in the central nervous system (CNS), where it is required to control HSV-1, which spreads from the epithelium to the CNS via cranial nerves. TLR3 is also expressed in epithelial and dendritic cells, which apparently use TLR3-independent pathways to prevent further dissemination of HSV-1 and to provide resistance to other pathogens in TLR3-deficient patients. Human TLR3 appears to be redundant in host defense to most microbes but is vital for natural immunity to HSV-1 in the CNS, which suggests that neurotropic viruses have contributed to the evolutionary maintenance of TLR3. | |||
| ALP9245 |
Recombinant Cynomolgus BDCA-2 Protein,Cynomolgus,N-His,Expi293 |
A0A2K5UWP4(Tyr48-Ile212) |
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| BDCA-2, BDCA-3, and BDCA-4. In blood, BDCA-2 and BDCA-4 are expressed on CD11c(-) CD123(bright) plasmacytoid dendritic cells, whereas BDCA-3 is expressed on small population of CD11c() CD123(-) dendritic cells. All three Ags are not detectable on a third blood dendritic cell population, which is CD1c() CD11c(bright) CD123(dim), or on any other cells in blood.BDCA-2 is completely down-regulated on plasmacytoid CD11c(-) CD123(bright) dendritic cells, BDCA-2 is rapidly internalized at 37 degrees C after mAb labeling. | |||
| ALP9247 |
Recombinant Cynomolgus BDCA-2 Protein,Cynomolgus,N-hFc,Expi293 |
A0A2K5UWP4(Tyr48-Ile212) |
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| BDCA-2, BDCA-3, and BDCA-4. In blood, BDCA-2 and BDCA-4 are expressed on CD11c(-) CD123(bright) plasmacytoid dendritic cells, whereas BDCA-3 is expressed on small population of CD11c() CD123(-) dendritic cells. All three Ags are not detectable on a third blood dendritic cell population, which is CD1c() CD11c(bright) CD123(dim), or on any other cells in blood.BDCA-2 is completely down-regulated on plasmacytoid CD11c(-) CD123(bright) dendritic cells, BDCA-2 is rapidly internalized at 37 degrees C after mAb labeling. | |||
