目录号 | 产品详情 | 靶点 | |
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T74267 | |||
STINGagonist-17 (compound 4a) 是一种有效的STING 激动剂,其IC50值为 0.062 nM,具有抗癌活性,可用于肿瘤免疫。 | |||
T81084 | |||
STINGagonist-18(compound 1a)适用于ADCs的合成,例如与Trastuzumab偶联。 | |||
T63458 | |||
STING agonist-11 是一种 STING 小分子环脲类的有效激活剂 (EC50: 18 nM)。STING 激活是一种具有高度潜力的免疫疗法。 | |||
T75095 | |||
STINGagonist-27 (CF509) 是一种非核苷酸小分子 STING 激动剂。STINGagonist-23 激活 STING,表现出抗 SARS-CoV 系列的活性。 | |||
T75091 | |||
STINGagonist-23 (CF502) 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。 | |||
T75093 | |||
STINGagonist-25 (CF505) 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。 | |||
T74328 | |||
STINGagonist-8 dihydrochloride (5-AB) 是一种有效STING 激动剂,在 THP1-Dual KI-hSTING-R232 细胞中的EC50为 27 nM。 | |||
T81082 | STING | ||
STING-IN-7(化合物 21),作为一种STING抑制剂,具有11.5 nM的IC50值,能够抑制STING与干扰素调节因子 3 (IRF3) 的磷酸化。 | |||
T75011 | STING | ||
STING-IN-5为有效STING抑制剂,IC50达1.15 μM,能在巨噬细胞内抑制LSP诱导之NO合成,从而抑制炎症反应,主用于抗炎疾病与败血症研究。 | |||
T61043 | |||
STING agonist-7 是一种非核苷酸STING 的激动剂,可选择性结合小鼠而非人类 STING。 |
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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