1. 重组蛋白
  2. Cytokines and Growth Factors
  3. TNF Superfamily
  4. TNF Receptor Superfamily

TNF Receptor Superfamily  (肿瘤坏死因子受体)

TNF 受体超家族 (TNFRSF) 成员是跨膜蛋白,细胞外区域富含半胱氨酸,与同源配体结合。大约 30个已经鉴定出肿瘤坏死因子受体超家族成员。肿瘤坏死因子受体 (TNFRs) 主要是 I 型跨膜蛋白,包含一个细胞外 TNF 结合区域和一个细胞质尾部。但 BCMA、TACI、BAFFR 和 XEDAR 属于 III 型跨膜蛋白[1]。TNFRs 分为三种类型:(1) 含有死亡域 (DD) 的受体 (脂肪酸合酶、TNFR1 和 DR3),它们通过 DD 引发的外部凋亡途径激活 caspase 级联;(2) 在胞质尾区包含一个或多个 TRAF 相互作用基序 (TIM),募集 TRAF 家族成员,最终激活多个信号转导通路的关键分子;(3) 不包含功能性细胞内信号结构域或者基序,可以与其它两组的受体竞争性的与相应配体结合[2]。TNFRSF 主要参与细胞凋亡和炎症反应,也参与细胞增殖、分化和存活[3][4]

TNF receptor superfamily (TNFRSF) members are transmembrane proteins cysteine-rich motifs in their extracellular domains that bind to their cognate ligands. About 30 members of TNFRSF members have been identified. Tumor necrosis factor receptors (TNFRs) are primarily type I transmembrane proteins containing an extracellular TNF binding region and a cytoplasmic tail. But BCMA, TACI, BAFFR and XEDAR belong to Type III transmembrane proteins[1]. TNFRs can be divided into three types: (1) receptors containing the death domain (DD) (fatty acid synthase, TNFR1, and DR3) activate caspase cascades via the external apoptotic pathway triggered by DD; (2) the cytoplasmic cauda region contains one or more TRAF interaction mods (TIM), which recruit TRAF family members and ultimately activate key molecules of multiple signal transduction pathways; (3) it does not contain functional intracellular signaling domain or motif, and can competitively bind to the corresponding ligand with the other two groups of receptors[2]. TNFRSF are primarily involved in apoptosis and inflammation, also and are also involved in cell proliferation, differentiation and survival[3][4].

目录号 产品名 / 同用名 种属 表达系统
  • HY-P76683
    TNFRII Protein, Human (257a.a, HEK293, His)

    TNFRII 蛋白, Human (257a.a, HEK293, His)

    TNF-R2; CD120b; Tumor necrosis factor receptor superfamily member 1b; p75; Tnfr2

    Human HEK293
    TNFRII (TNFRSF1B) 蛋白具有与肿瘤坏死因子-α (TNF-α) 高度结合的能力。TNFRII 具有促凋亡作用。TNFRII 招募 TRAF2,诱导基因表达并与 TNFRI 进行密集串扰。TNFRII 选择性地增强死亡受体 TNFRII 诱导的细胞凋亡。TNFRII Protein, Human (257a.a, HEK293, His) 由 HEK293 细胞表达,具有跨膜区 (M1-D257),C 端带有 His 标签。
  • HY-P72025
    TNFRII Protein, Human (HEK293, hFc)

    TNFRII 蛋白, Human (HEK293, hFc)

    Tumor necrosis factor receptor 2; TNF-R2; Tumor necrosis factor receptor type II; TNF-RII; TNFR-II; p75; p80 TNF-alpha receptor; CD120b; Etanercept; TBP-2; TBPII;

    Human HEK293
    TNFRII (TNFRSF1B) 蛋白具有与肿瘤坏死因子-α (TNF-α) 高度结合的能力。TNFRII 具有促凋亡作用。TNFRII 招募 TRAF2,诱导基因表达并与 TNFRI 进行密集串扰。TNFRII 选择性地增强死亡受体 TNFRII 诱导的细胞凋亡。TNFRII Protein, Human (HEK293, hFc) 由 HEK293 细胞表达,具有跨膜区 (L23-D257),C 端带有 hFc 标签。
  • HY-P7271
    NGFR Protein, Human (HEK293)

    重组人 NGFR 蛋白 (HEK293, Fc)

    rHuNGFR; Gp80-LNGFR; p75 ICD; CD271; TNFRSF16

    Human HEK293
    Nerve Growth Factor Receptor (NGFR) 也称为 CD271、p75NTR、TNFRSF16,是神经营养蛋白家族的跨膜低亲和力受体。NGFR 没有内在的酪氨酸激酶活性。NGFR 可作为肿瘤抑制因子,负向调节细胞生长和增殖。NGF-NGFR 激活 NF-κB,从而抑制细胞凋亡,增加神经鞘瘤和乳腺癌细胞的存活率。NGFR Protein, Human (HEK293) 是一种由 HEK293 细胞表达的重组蛋白,由 222 个 (K29-N250) 氨基酸组成。
  • HY-P70806
    TRAIL R2/TNFRSF10B Protein, Human (127a.a, HEK293, His)

    Tumor Necrosis Factor Receptor Superfamily Member 10B; Death Receptor 5; TNF-Related Apoptosis-Inducing Ligand Receptor 2; TRAIL Receptor 2; TRAIL-R2; CD262; TNFRSF10B; DR5; KILLER; TRAILR2; TRICK2; ZTNFR9

    Human HEK293
    TRAIL R2/TNFRSF10B 蛋白是 TNFSF10/TRAIL 的受体,通过 FADD 招募 caspase-8 来启动细胞凋亡。它形成死亡诱导信号复合物 (DISC),激活半胱天冬酶并介导细胞凋亡。TRAIL R2/TNFRSF10B Protein, Human (127a.a, HEK293, His) 是重组的 TRAIL R2/TNFRSF10B 蛋白,由 HEK293 表达,带有 C-6*His 标签。TRAIL R2/TNFRSF10B Protein, Human (127a.a, HEK293, His) 全长 127 个氨基酸,分子量约为 ~18.0 kDa。
  • HY-P7168
    Fas/CD95 Protein, Human (HEK293)

    重组人 Fas/CD95 蛋白 (HEK293)

    rHuFASR/TNFRSF6; Tumor necrosis factor receptor superfamily member 6; Fas receptor; CD95; APT1; FAS1; Apo-1

    Human HEK293
    Fas 受体是一种细胞表面死亡受体,又称凋亡介导表面抗原 Fas 和 Apo-1 抗原。Fas 受体与 Fas 配体结合而形成死亡诱导信号复合物,如 Fas 相关死亡结构域蛋白 (FADD)。Fas 受体参与 caspase 级联反应,调节下游 JNK 和 p38-K 的激活。它还介入 ERK/JNK MAPKs 信号级联,激活 MAPK3/ERK1, MAPK8/JNKNF-κB,与多种恶性肿瘤和免疫系统疾病的发病机制有关。人 Fas 受体含有一个死亡结构域 (230-314 a.a.),在调节程序性死亡中发挥关键作用。重组人 Fas/CD95 蛋白 (HEK293) 全长 157 个氨基酸 (Q26-S172),由 HEK293 细胞表达,不带标签。
  • HY-P72847
    BCMA/TNFRSF17 Protein, Human (HEK293, His)

    重组人 BCMA/TNFRSF17 蛋白 (HEK293, His)

    Tumor necrosis factor receptor superfamily member 17; CD269; TNFRSF17; BCM; BCMA

    Human HEK293
    B Cell Maturation Antigen (BCMA) 也称为 TNFRSF17 或 CD269,是肿瘤坏死因子受体 (TNFR) 超家族的跨膜糖蛋白成员。BCMA 用作多发性骨髓瘤 (MM) 的生物标志物。BCMA 主要在 B 细胞增殖、存活以及分化为浆细胞方面发挥重要作用。BCMA/TNFRSF17 Protein, Human (HEK293, His) 是一种由 HEK293 细胞表达重组蛋白,其 C 末端带有 His 标签,由 54 (M1-A54) 个氨基酸组成。
  • HY-P7317
    4-1BB/TNFRSF9 Protein, Human (CHO, Fc)

    重组人 4-1BB/TNFRSF9 蛋白 (CHO, Fc)

    rHu4-1BB, Fc Chimera; CD137; ILA

    Human CHO
    4-1BB (CD137; TNFRSF9),是 TNFSF9/4-1BBL 的受体,属于肿瘤坏死因子 (TNF) 受体超家族。4-1BB 有助于T细胞的激活和发育,还诱导外周单核细胞增殖、向肿瘤微环境迁移。4-1BB 也参与增强 Nrf2 和 NF-κB 通路介导的内皮细胞凋亡。人的 4-1BB 蛋白是一种表面糖蛋白,具有一个跨膜结构域 (187-213 a.a.)。重组人 4-1BB/TNFRSF9 蛋白 (CHO, Fc) 是 4-1BB 蛋白的胞外部分 (L24-Q186),由 HEK293 细胞表达,带有 C 端 hFc 标签。
  • HY-P73499A
    CD40 Protein, Human (193a.a, HEK293, C-His)

    Tumor Necrosis Factor Receptor Superfamily member 5; Bp50; CD40L Receptor; CDw40; TNFRSF5

    Human HEK293
    CD40 蛋白是一种 TNFSF5/CD40LG 受体,通过 TRAF6 和 MAP3K8 介导的途径转导信号,激活巨噬细胞和 B 细胞中的 ERK,并诱导免疫球蛋白分泌。CD40 以单体和同二聚体形式存在,并与 TRAF 蛋白(TRAF1、TRAF2、TRAF3、TRAF5 和 TRAF6)相互作用。CD40 Protein, Human (193a.a, HEK293, C-His) 是重组的 CD40 蛋白,由 HEK293 表达,带有 C-6*His 标签。CD40 Protein, Human (193a.a, HEK293, C-His) 全长 173 个氨基酸,分子量约为 ~28-32 kDa。
  • HY-P7646
    BAFFR/TNFRSF13C Protein, Mouse (HEK293, Fc)

    重组小鼠 BAFFR/TNFRSF13C 蛋白 (HEK293, Fc)

    rMuBAFFR/TNFRSF13C, C-Fc; BAFF R; BAFFR; BR3; CD268; TNFRSF13C

    Mouse HEK293
    BAFF Receptor (B-cell activating factor receptor,BAFF-R),又名 TNFRSF13C 和BR3,是识别 BAFF 的 TNF 受体超家族的一种膜蛋白。BAFF Receptor 是 B 细胞存活的关键受体,也是 B 细胞和 T 细胞活化的有效共刺激因子。BAFFR/TNFRSF13C Protein, Mouse (HEK293, Fc) 是一种由 HEK293 细胞表达的重组蛋白,其 C 末端带有 His 标签,由 62 个 (S10-A71) 氨基酸组成。
  • HY-P77100
    NGFR Protein, Mouse (HEK293, Fc)

    重组小鼠 NGFR 蛋白 (HEK293, Fc)

    NGFR; Gp80-LNGFR; p75 ICD; CD271; TNFRSF16

    Mouse HEK293
    Nerve Growth Factor Receptor (NGFR) 也称为 CD271、p75NTR、TNFRSF16,是神经营养蛋白家族的跨膜低亲和力受体。NGFR 没有内在的酪氨酸激酶活性。NGFR 可作为肿瘤抑制因子,负向调节细胞生长和增殖。NGF-NGFR 激活 NF-κB,从而抑制细胞凋亡,增加神经鞘瘤和乳腺癌细胞的存活率。NGFR Protein, Mouse (HEK293, Fc) 是一种由 HEK293 细胞表达的重组蛋白,其 C 末端带有 Fc 标签,由 243 (M1-N243) 个氨基酸组成。
  • HY-P78065
    BAFFR/TNFRSF13C Protein, Human (Biotinylated, HEK293, His-Avi)

    重组人 BAFFR/TNFRSF13C 蛋白 (Biotinylated, HEK293, His-Avi)

    CD268; BAFFR; BR3; TNFRSF13C; BROMIX; CVID4; prolixin

    Human HEK293
    BAFF Receptor (B-cell activating factor receptor,BAFF-R),又名 TNFRSF13C 和BR3,是识别 BAFF 的 TNF 受体超家族的一种膜蛋白。BAFF Receptor 是 B 细胞存活的关键受体,也是 B 细胞和 T 细胞活化的有效共刺激因子。AFFR/TNFRSF13C Protein, Human (Biotinylated, HEK293, His-Avi) 是一种由 HEK293 细胞表达的生物素化的重组蛋白,其 C 末端带有一个 Avi 标签和一个 His 标签,由 65 个 (S7-A71) 氨基酸组成。
  • HY-P78070
    BCMA/TNFRSF17 Protein, Human (Biotinylated, HEK293, His-Avi)

    重组人 BCMA/TNFRSF17 蛋白 (Biotinylated, HEK293, His-Avi)

    CD269; TNFRSF17; BCMA; BCM; TNFRSF13A

    Human HEK293
    B Cell Maturation Antigen (BCMA) 也称为 TNFRSF17 或 CD269,是肿瘤坏死因子受体 (TNFR) 超家族的跨膜糖蛋白成员。BCMA 用作多发性骨髓瘤 (MM) 的生物标志物。BCMA 主要在 B 细胞增殖、存活以及分化为浆细胞方面发挥重要作用。BCMA/TNFRSF17 Protein, Human (Biotinylated, HEK293, His-Avi) 是一种由 HEK293 细胞表达的生物素化的重组蛋白,其 C 末端带有一个 Avi 标签和一个 His 标签,由 54 (M1-A54) 个氨基酸组成。
  • HY-P78071
    BCMA/TNFRSF17 Trimer Protein, Human (Biotinylated, HEK293, His-Avi)

    重组人 BCMA/TNFRSF17 蛋白 (Biotinylated, HEK293, His-Avi)

    CD269; TNFRSF17; BCMA; BCM; TNFRSF13A

    Human HEK293
    B Cell Maturation Antigen (BCMA) 也称为 TNFRSF17 或 CD269,是肿瘤坏死因子受体 (TNFR) 超家族的跨膜糖蛋白成员。BCMA 用作多发性骨髓瘤 (MM) 的生物标志物。BCMA 主要在 B 细胞增殖、存活以及分化为浆细胞方面发挥重要作用。BCMA/TNFRSF17 Trimer Protein, Human (Biotinylated, HEK293, His-Avi) 是一种由 HEK293 细胞表达的生物素化的重组蛋白,其 C 末端带有一个 Avi 标签和一个 His 标签,由 54 (M1-A54) 个氨基酸组成。
  • HY-P78091
    CD40 Protein, Human (Biotinylated, HEK293, His-Avi)

    CD40; CD40L receptor; TNFRSF5; B cell surface antigen CD40; B-cell surface antigen CD40; Bp50B cell-associated molecule; CD40 antigen; CD40 molecule, TNF receptor superfamily member 5; CD40 type II isoform; CDw40; MGC9013; nerve growth factor receptor-relat

    Human HEK293
    CD40 蛋白是一种 TNFSF5/CD40LG 受体,通过 TRAF6 和 MAP3K8 介导的途径转导信号,激活巨噬细胞和 B 细胞中的 ERK,并诱导免疫球蛋白分泌。CD40 以单体和同二聚体形式存在,并与 TRAF 蛋白(TRAF1、TRAF2、TRAF3、TRAF5 和 TRAF6)相互作用。CD40 Protein, Human (Biotinylated, HEK293, His-Avi) 是重组的 CD40 蛋白,由 HEK293 表达,带有 C-Avi, C-His 标签。CD40 Protein, Human (Biotinylated, HEK293, His-Avi) 全长 173 个氨基酸,分子量为 35-40 kDa。
  • HY-P78189
    OX40/TNFRSF4 Protein, Human (Biotinylated, HEK293, His-Avi)

    重组人 OX40/TNFSF4 蛋白 (生物素化, HEK293, His-Avi)

    CD134; OX40; OX40L receptor; TNFRSF4; ACT-135; Ly-70; OX40 homologue;  TXGP1L; IMD16

    Human HEK293
    OX40 (TNFRSF4) 是 OX40 配体的受体。OX40 常在 T 细胞上表达。OX40 Ligand 可以激活 OX40,从而扮演 T 细胞共刺激分子的角色。OX40-OX40 Ligand 之间的相互作用可促进效应 T 细胞存活并有效地诱导记忆 T 细胞生成,以及增强 Tfh 细胞对 B 细胞的辅助功能、促进 DCs 的分化和成熟。OX40/TNFRSF4 Protein, Human (Biotinylated, HEK293, His-Avi) 是一种由 HEK293 产生的生物素化的重组人 OX40 (L29-A216),C 端带 Avi 和 His 标签。
  • HY-P78219
    TRAIL R1/TNFRSF10A Protein, Human (Biotinylated, HEK293, His-Avi)

    DR4; CD261; TNFRSF10A; TRAIL-R; APO2; TRAIL R1; MGC9365

    Human HEK293
    TRAIL R1/TNFRSF10A 蛋白是 TNFSF10/TRAIL 的受体,它通过 FADD 招募 caspase-8,启动细胞凋亡并形成死亡诱导信号复合物 (DISC)。它激活 NF-kappa-B 并与单体状态下的 TRADD 和 RIPK1 相互作用。TRAIL R1/TNFRSF10A Protein, Human (Biotinylated, HEK293, His-Avi) 是重组的 TRAIL R1/TNFRSF10A 蛋白,由 HEK293 表达,带有 C-Avi, C-His 标签。TRAIL R1/TNFRSF10A Protein, Human (Biotinylated, HEK293, His-Avi) 全长 206 个氨基酸,分子量为 25-30 kDa。
  • HY-P78220
    TRAIL R2/TNFRSF10B Protein, Human (Biotinylated, HEK293, His-Avi)

    CD262; DR5; DR5TRICK2B; Fas-like protein; KILLER/DR5; TNFRSF10B; TRAIL R2; TRAIL receptor 2; TRAILR2; TRICK2; TRICK2A; TRICKB; ZTNFR9; KILLER

    Human HEK293
    TRAIL R2/TNFRSF10B 蛋白是 TNFSF10/TRAIL 的受体,通过 FADD 招募 caspase-8 来启动细胞凋亡。它形成死亡诱导信号复合物 (DISC),激活半胱天冬酶并介导细胞凋亡。TRAIL R2/TNFRSF10B Protein, Human (Biotinylated, HEK293, His-Avi) 是重组的 TRAIL R2/TNFRSF10B 蛋白,由 HEK293 表达,带有 C-Avi, C-His 标签。TRAIL R2/TNFRSF10B Protein, Human (Biotinylated, HEK293, His-Avi) 全长 127 个氨基酸,分子量为 20-25 kDa。
  • HY-P78221
    TRAILR4/TNFRSF10D Protein, Human (Biotinylated, HEK293, His-Avi)

    CD264; RSF10D; TRAILR4; DCR2; TRUNDD; TNFRSF10D

    Human HEK293
    TRAILR4/TNFRSF10D 蛋白是 TRAIL 的受体,由于死亡结构域被截短,因此缺乏诱导细胞凋亡的能力。矛盾的是,它不仅不能诱导细胞凋亡,而且还能阻止 TRAIL 介导的细胞凋亡。TRAILR4/TNFRSF10D Protein, Human (Biotinylated, HEK293, His-Avi) 是重组的 TRAILR4/TNFRSF10D 蛋白,由 HEK293 表达,带有 C-Avi, C-His 标签。TRAILR4/TNFRSF10D Protein, Human (Biotinylated, HEK293, His-Avi) 全长 156 个氨基酸,分子量为 38-50 kDa。
  • HY-P70805
    TNFRSF11B/OPG Protein, Human (HEK293, His)

    重组人 TNFRSF11B/OPG 蛋白 (HEK293, His)

    Tumor Necrosis Factor Receptor Superfamily Member 11B; Osteoclastogenesis Inhibitory Factor; Osteoprotegerin; TNFRSF11B; OCIF; OPG

    Human HEK293
    Osteoprotegerin (OPG) 属于 TNF 受体超家族。OPG 在许多组织中表达,包括心脏、肾脏、肝脏、脾脏和骨髓。Osteoprotegerin 具有骨保护作用,在骨重塑中起关键作用。Osteoprotegerin 可与 RANKL 结合,以抑制 TNFSF11 与 RANKL 的结合,从而中和 RANKL 在破骨细胞生成中的作用。OPG 还参与癌症的许多生物过程。TNFRSF11B/OPG Protein, Human (HEK293, His) 是一种由 HEK293 产生的重组人 TNFRSF11B/OPG (E22-L401),C 端带 6*His 标签。
  • HY-P70815
    TNFRSF10C Protein, Human (HEK293, His)

    Tumor Necrosis Factor Receptor Superfamily Member 10C; Antagonist Decoy Receptor for TRAIL/Apo-2L; Decoy TRAIL Receptor Without Death Domain; Decoy Receptor 1; DcR1; Lymphocyte Inhibitor of TRAIL; TNF-Related Apoptosis-Inducing Ligand Receptor 3; TRAIL Receptor

    Human HEK293
    TNFRSF10C 蛋白是 TRAIL 的受体,缺乏细胞质死亡结构域,因此无法诱导细胞凋亡。相反,它通过竞争与 TRAIL-R1 和 R2 的配体结合来保护细胞,充当诱饵受体并减轻 TRAIL 介导的细胞凋亡。TNFRSF10C Protein, Human (HEK293, His) 是重组的 TNFRSF10C 蛋白,由 HEK293 表达,带有 C-6*His 标签。TNFRSF10C Protein, Human (HEK293, His) 全长 196 个氨基酸,分子量为 50-60 kDa。
目录号 产品名 作用方式 纯度

Following the binding of TNF to TNF receptors, TNFR1 binds to TRADD, which recruits RIPK1, TRAF2/5 and cIAP1/2 to form TNFR1 signaling complex I; TNFR2 binds to TRAF1/2 directly to recruit cIAP1/2. Both cIAP1 and cIAP2 are E3 ubiquitin ligases that add K63 linked polyubiquitin chains to RIPK1 and other components of the signaling complex. The ubiquitin ligase activity of the cIAPs is needed to recruit the LUBAC, which adds M1 linked linear polyubiquitin chains to RIPK1. K63 polyubiquitylated RIPK1 recruits TAB2, TAB3 and TAK1, which activate signaling mediated by JNK and p38, as well as the IκB kinase complex. The IKK complex then activates NF-κB signaling, which leads to the transcription of anti-apoptotic factors-such as FLIP and Bcl-XL-that promote cell survival. 

 

The formation of TNFR1 complex IIa and complex IIb depends on non-ubiquitylated RIPK1. For the formation of complex IIa, ubiquitylated RIPK1 in complex I is deubiquitylated by CYLD. This deubiquitylated RIPK1 dissociates from the membrane-bound complex and moves into the cytosol, where it interacts with TRADD, FADD, Pro-caspase 8 and FLIPL to form complex IIa. By contrast, complex IIb is formed when the RIPK1 in complex I is not ubiquitylated owing to conditions that have resulted in the depletion of cIAPs, which normally ubiquitylate RIPK1. This non-ubiquitylated RIPK1 dissociates from complex I, moves into the cytosol, and assembles with FADD, Pro-caspase 8, FLIPL and RIPK3 (but not TRADD) to form complex IIb. For either complex IIa or complex IIb to prevent necroptosis, both RIPK1 and RIPK3 must be inactivated by the cleavage activity of the Pro-caspase 8-FLIPL heterodimer or fully activated caspase 8. The Pro-caspase 8 homodimer generates active Caspase 8, which is released from complex IIa and complex IIb. This active Caspase 8 then carries out cleavage reactions to activate downstream executioner caspases and thus induce classical apoptosis. 

 

Formation of the complex IIc (necrosome) is initiated either by RIPK1 deubiquitylation mediated by CYLD or by RIPK1 non-ubiquitylation due to depletion of cIAPs, similar to complex IIa and complex IIb formation. RIPK1 recruits numerous RIPK3 molecules. They come together to form amyloid microfilaments called necrosomes. Activated RIPK3 phosphorylates and recruits MLKL, eventually leading to the formation of a supramolecular protein complex at the plasma membrane and necroptosis [1][2].

 

Reference:
[1]. Brenner D, et al. Regulation of tumour necrosis factor signalling: live or let die.Nat Rev Immunol. 2015 Jun;15(6):362-74. 
[2]. Conrad M, et al. Regulated necrosis: disease relevance and therapeutic opportunities.Nat Rev Drug Discov. 2016 May;15(5):348-66.