目录号 | 产品详情 | 靶点 | |
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T75092 | |||
STINGagonist-24 (CF504) 是一种非核苷酸小分子STING 激动剂。STINGagonist-23 激活STING,增加STING、TBK1和IRF3的磷酸化。STINGagonist-23 可促进肿瘤细胞中IFN-β、IL-6、CXCL-10、TNF-α、ISG-15和CCL-5的水平。STINGagonist-23 表现出抗SARS-CoV 系列的活性。 | |||
T75090 | |||
STINGagonist-22 (CF501) 是一种有效的非核苷酸STING 激动剂。STINGagonist-22 是一种佐剂,通过激活STING 来诱导 I 型干扰素 (IFN-I) 反应和促炎细胞因子的产生。STINGagonist-22 可用作增强原始蛋白疫苗的佐剂,产生有效、广泛和长期的免疫保护。STINGagonist-22 可用于 SARS-CoV-2 变异和 sarbecovirus 疾病研究。 | |||
T83775 | |||
STING激动剂12L是一种刺激干扰素基因(STING)的激动剂。它与野生型STING结合(IC50 = 1.15 µM),以及STING的R232、AQ和Q变体(IC50分别为1.06、0.61和1.12 µM),并在THP-1和RAW 264.7细胞中诱导报告基因表达(EC50分别为0.38和12.94 µM)。STING激动剂12L (5 µM)在THP-1细胞中诱导IFNB1、CXCL10和IL6 mRNA的表达。在体内,STING激动剂12L (10 mg/kg)提高了血浆IFN-β水平,并且在B16/F10小鼠黑色素瘤模型中减少了肿瘤体积和肺转移灶的数量。 | |||
T83841 | |||
STING激动剂D61(D61)是干扰素基因刺激剂(STING)的激动剂。它在基于细胞的分析中诱导IFN3诱导的分泌性碱性磷酸酶(SEAP)报告基因和IFN-β诱导的报告基因的表达(EC50分别为52.9和116 nM)。D61(4, 6, 和8 µM)增加了编码IFN-β和化学因子(C-X-C基序)配体10(CXCL10)的mRNA的表达以及TANK结合激酶1(TBK1)、IRF3和STING在THP-1单核细胞中的磷酸化。在体内,D61(每隔一天0.25 mg/kg)在CT26小鼠结肠癌模型中减少肿瘤体积,而不影响体重。 | |||
T75161 | |||
STINGagonist-31 是一种 STING 激动剂,对 h-STING 和 m-STING 的 EC50值为 0.24 和 39.51 μM。STINGagonist-31 具有抗肿瘤功效。 | |||
T74621 | |||
STINGagonist-9 (Compound 45) 是一种有效的STING 激动剂,对 h-STING 和 m-STING 的EC50值分别为 1.2 nM 和 32.82 μM。STINGagonist-9 具有抗肿瘤活性。 | |||
T75094 | |||
STINGagonist-26 (CF508) 是一种非核苷酸小分子STING 激动剂。STINGagonist-23 激活STING,增加STING、TBK1和IRF3的磷酸化。STINGagonist-23 可促进肿瘤细胞中IFN-β、IL-6、CXCL-10、TNF-α、ISG-15和CCL-5的水平。STINGagonist-23 表现出抗SARS-CoV 系列的活性。 | |||
T74268 | |||
STINGagonist-13 是一种STING 激动剂,通过STING 介导的免疫激活进行癌症免疫。STINGagonist-13 可刺激STING 下游信号传导并促进 I 型干扰素免疫反应。STINGagonist-13 能显著降低肿瘤体积并具有免疫记忆衍生的癌症抑制活性。 | |||
T75096 | |||
STINGagonist-28 (CF510) 是一种非核苷酸小分子STING 激动剂。STINGagonist-23 激活STING,增加STING、TBK1和IRF3的磷酸化。STINGagonist-23 可促进肿瘤细胞中IFN-β、IL-6、CXCL-10、TNF-α、ISG-15和CCL-5的水平。STINGagonist-23 表现出抗SARS-CoV 系列的活性。 | |||
T81083 | |||
STINGagonist-19 用于 ISAC(immune-stimulating antibody conjugates)分子的合成。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPJ-01206 | Sting Protein, Human, Recombinant (Sumo & His) | Human | E. coli | ||
Stimulator of Interferon Gene(Sting,TMEM173) belongs to the TMEM173 family. STING is 379 amino acids (aa) in length. It contains an N-terminal cytoplasmic region (aa 1-20), four transmembrane segments (aa 21-173), and a C-terminal cytoplasmic domain (aa 174-379). It ubiquitously expressed in skin endothelial cells, alveolar type 2 pneumocytes, bronchial epithelium and alveolar macrophagesand. Its subunit structure associated with the MHC-II complex and Interacts with DDX58/RIG-I, MAVS and SSR2, RNF5 and TRIM56 along with TBK1. This type of protein often uses as facilitator of innate immune signaling that acts as a sensor of cytosolic DNA from bacteria and viruses and promotes the production of type I interferon.
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TMPH-01836 | Human Papilloma Virus type 18 (HPV 18) Protein E7 (E. coli, His) | HPV 18 | E. coli | ||
Plays a role in viral genome replication by driving entry of quiescent cells into the cell cycle. Stimulation of progression from G1 to S phase allows the virus to efficiently use the cellular DNA replicating machinery to achieve viral genome replication. E7 protein has both transforming and trans-activating activities. Induces the disassembly of the E2F1 transcription factor from RB1, with subsequent transcriptional activation of E2F1-regulated S-phase genes. Interferes with host histone deacetylation mediated by HDAC1 and HDAC2, leading to transcription activation. Plays also a role in the inhibition of both antiviral and antiproliferative functions of host interferon alpha. Interaction with host TMEM173/STING impairs the ability of TMEM173/STING to sense cytosolic DNA and promote the production of type I interferon (IFN-alpha and IFN-beta).
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TMPH-01834 | Human Papilloma Virus type 16 (HPV 16) Protein E7 (His) | HPV 16 | E. coli | ||
Plays a role in viral genome replication by driving entry of quiescent cells into the cell cycle. Stimulation of progression from G1 to S phase allows the virus to efficiently use the cellular DNA replicating machinery to achieve viral genome replication. E7 protein has both transforming and trans-activating activities. Induces the disassembly of the E2F1 transcription factor from RB1, with subsequent transcriptional activation of E2F1-regulated S-phase genes. Interferes with host histone deacetylation mediated by HDAC1 and HDAC2, leading to transcription activation. Plays also a role in the inhibition of both antiviral and antiproliferative functions of host interferon alpha. Interaction with host TMEM173/STING impairs the ability of TMEM173/STING to sense cytosolic DNA and promote the production of type I interferon (IFN-alpha and IFN-beta).
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TMPH-00067 | Venom dipeptidyl peptidase 4 Protein, Apis mellifera, Recombinant (His & Myc) | Apis mellifera | E. coli | ||
Venom dipeptidyl-peptidase which removes N-terminal dipeptides sequentially from polypeptides having unsubstituted N-termini provided that the penultimate residue is proline. May process promelittin into its active form and/or modulate the chemotactic activity of immune cells after the insect sting.
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TMPH-01827 | Human Papilloma Virus type 11 (HPV 11) Protein E7 (His & Myc) | HPV 11 | E. coli | ||
Plays a role in viral genome replication by driving entry of quiescent cells into the cell cycle. Stimulation of progression from G1 to S phase allows the virus to efficiently use the cellular DNA replicating machinery to achieve viral genome replication. E7 protein has both transforming and trans-activating activities. Induces the disassembly of the E2F1 transcription factor from RB1, with subsequent transcriptional activation of E2F1-regulated S-phase genes. Interferes with host histone deacetylation mediated by HDAC1 and HDAC2, leading to transcription activation. Plays also a role in the inhibition of both antiviral and antiproliferative functions of host interferon alpha. Interaction with host TMEM173/STING impairs the ability of TMEM173/STING to sense cytosolic DNA and promote the production of type I interferon (IFN-alpha and IFN-beta).
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TMPH-01837 | Human Papilloma Virus type 18 (HPV 18) Protein E7 (His) | HPV 18 | Yeast | ||
Plays a role in viral genome replication by driving entry of quiescent cells into the cell cycle. Stimulation of progression from G1 to S phase allows the virus to efficiently use the cellular DNA replicating machinery to achieve viral genome replication. E7 protein has both transforming and trans-activating activities. Induces the disassembly of the E2F1 transcription factor from RB1, with subsequent transcriptional activation of E2F1-regulated S-phase genes. Interferes with host histone deacetylation mediated by HDAC1 and HDAC2, leading to transcription activation. Plays also a role in the inhibition of both antiviral and antiproliferative functions of host interferon alpha. Interaction with host TMEM173/STING impairs the ability of TMEM173/STING to sense cytosolic DNA and promote the production of type I interferon (IFN-alpha and IFN-beta).
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TMPH-01838 | Human Papilloma Virus type 52 (HPV 52) Protein E7 (His & SUMO) | HPV 52 | E. coli | ||
Plays a role in viral genome replication by driving entry of quiescent cells into the cell cycle. Stimulation of progression from G1 to S phase allows the virus to efficiently use the cellular DNA replicating machinery to achieve viral genome replication. E7 protein has both transforming and trans-activating activities. Induces the disassembly of the E2F1 transcription factor from RB1, with subsequent transcriptional activation of E2F1-regulated S-phase genes. Interferes with host histone deacetylation mediated by HDAC1 and HDAC2, leading to transcription activation. Plays also a role in the inhibition of both antiviral and antiproliferative functions of host interferon alpha. Interaction with host TMEM173/STING impairs the ability of TMEM173/STING to sense cytosolic DNA and promote the production of type I interferon (IFN-alpha and IFN-beta).
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TMPH-00900 | Human adenovirus C serotype 5 Early E1A protein (His & SUMO) | HAdV-5 | E. coli | ||
Plays a role in viral genome replication by driving entry of quiescent cells into the cell cycle. Stimulation of progression from G1 to S phase allows the virus to efficiently use the cellular DNA replicating machinery to achieve viral genome replication. E1A protein has both transforming and trans-activating activities. Induces the disassembly of the E2F1 transcription factor from RB1 by direct competition for the same binding site on RB1, with subsequent transcriptional activation of E2F1-regulated S-phase genes and of the E2 region of the adenoviral genome. Release of E2F1 leads to the ARF-mediated inhibition of MDM2 and causes TP53/p53 to accumulate because it is not targeted for degradation by MDM2-mediated ubiquitination anymore. This increase in TP53, in turn, would arrest the cell proliferation and direct its death but this effect is counteracted by the viral protein E1B-55K. Inactivation of the ability of RB1 to arrest the cell cycle is critical for cellular transformation, uncontrolled cellular growth and proliferation induced by viral infection. Interaction with RBX1 and CUL1 inhibits ubiquitination of the proteins targeted by SCF(FBXW7) ubiquitin ligase complex, and may be linked to unregulated host cell proliferation. The tumorigenesis-restraining activity of E1A may be related to the disruption of the host CtBP-CtIP complex through the CtBP binding motif. Interaction with host TMEM173/STING impairs the ability of TMEM173/STING to sense cytosolic DNA and promote the production of type I interferon (IFN-alpha and IFN-beta). Promotes the sumoylation of host ZBED1/hDREF with SUMO1.
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TMPH-02314 | XRCC5 Protein, Human, Recombinant (His & MBP) | Human | Baculovirus | ||
Single-stranded DNA-dependent ATP-dependent helicase that plays a key role in DNA non-homologous end joining (NHEJ) by recruiting DNA-PK to DNA. Required for double-strand break repair and V(D)J recombination. Also has a role in chromosome translocation. The DNA helicase II complex binds preferentially to fork-like ends of double-stranded DNA in a cell cycle-dependent manner. It works in the 3'-5' direction. During NHEJ, the XRCC5-XRRC6 dimer performs the recognition step: it recognizes and binds to the broken ends of the DNA and protects them from further resection. Binding to DNA may be mediated by XRCC6. The XRCC5-XRRC6 dimer acts as regulatory subunit of the DNA-dependent protein kinase complex DNA-PK by increasing the affinity of the catalytic subunit PRKDC to DNA by 100-fold. The XRCC5-XRRC6 dimer is probably involved in stabilizing broken DNA ends and bringing them together. The assembly of the DNA-PK complex to DNA ends is required for the NHEJ ligation step. The XRCC5-XRRC6 dimer probably also acts as a 5'-deoxyribose-5-phosphate lyase (5'-dRP lyase), by catalyzing the beta-elimination of the 5' deoxyribose-5-phosphate at an abasic site near double-strand breaks. XRCC5 probably acts as the catalytic subunit of 5'-dRP activity, and allows to 'clean' the termini of abasic sites, a class of nucleotide damage commonly associated with strand breaks, before such broken ends can be joined. The XRCC5-XRRC6 dimer together with APEX1 acts as a negative regulator of transcription. In association with NAA15, the XRCC5-XRRC6 dimer binds to the osteocalcin promoter and activates osteocalcin expression. As part of the DNA-PK complex, involved in the early steps of ribosome assembly by promoting the processing of precursor rRNA into mature 18S rRNA in the small-subunit processome. Binding to U3 small nucleolar RNA, recruits PRKDC and XRCC5/Ku86 to the small-subunit processome. Plays a role in the regulation of DNA virus-mediated innate immune response by assembling into the HDP-RNP complex, a complex that serves as a platform for IRF3 phosphorylation and subsequent innate immune response activation through the cGAS-STING pathway.
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TMPH-02315 | XRCC5 Protein, Human, Recombinant (His & Myc) | Human | E. coli | ||
Single-stranded DNA-dependent ATP-dependent helicase that plays a key role in DNA non-homologous end joining (NHEJ) by recruiting DNA-PK to DNA. Required for double-strand break repair and V(D)J recombination. Also has a role in chromosome translocation. The DNA helicase II complex binds preferentially to fork-like ends of double-stranded DNA in a cell cycle-dependent manner. It works in the 3'-5' direction. During NHEJ, the XRCC5-XRRC6 dimer performs the recognition step: it recognizes and binds to the broken ends of the DNA and protects them from further resection. Binding to DNA may be mediated by XRCC6. The XRCC5-XRRC6 dimer acts as regulatory subunit of the DNA-dependent protein kinase complex DNA-PK by increasing the affinity of the catalytic subunit PRKDC to DNA by 100-fold. The XRCC5-XRRC6 dimer is probably involved in stabilizing broken DNA ends and bringing them together. The assembly of the DNA-PK complex to DNA ends is required for the NHEJ ligation step. The XRCC5-XRRC6 dimer probably also acts as a 5'-deoxyribose-5-phosphate lyase (5'-dRP lyase), by catalyzing the beta-elimination of the 5' deoxyribose-5-phosphate at an abasic site near double-strand breaks. XRCC5 probably acts as the catalytic subunit of 5'-dRP activity, and allows to 'clean' the termini of abasic sites, a class of nucleotide damage commonly associated with strand breaks, before such broken ends can be joined. The XRCC5-XRRC6 dimer together with APEX1 acts as a negative regulator of transcription. In association with NAA15, the XRCC5-XRRC6 dimer binds to the osteocalcin promoter and activates osteocalcin expression. As part of the DNA-PK complex, involved in the early steps of ribosome assembly by promoting the processing of precursor rRNA into mature 18S rRNA in the small-subunit processome. Binding to U3 small nucleolar RNA, recruits PRKDC and XRCC5/Ku86 to the small-subunit processome. Plays a role in the regulation of DNA virus-mediated innate immune response by assembling into the HDP-RNP complex, a complex that serves as a platform for IRF3 phosphorylation and subsequent innate immune response activation through the cGAS-STING pathway.
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