目录号 | 产品详情 | 靶点 | |
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T28832 | |||
SPC-839 is an IKK-2 Inhibitor with oral activity. | |||
T23191 | Others | ||
IκB kinase (IKK) inhibitor | |||
T15243 | Phosphatase PPAR | ||
Ertiprotafib is a PTP1B, IkB kinase β (IKK-β), and a dual PPARα and PPARβ agonist inhibitor ( IC50s: 1.6 μM for PTP1B, 400 nM for IKK-β, an EC50 of ~1 μM for PPARα/PPARβ). | |||
T27615 | |||
iNUB is a NEMO-Ub binding inhibitor. iNUB inhibits TNFα induced NF-κB signaling and has selectively toxic to IKK/NF-κB dependent ABC-DLBCL. | |||
TP1615 | |||
A cell-permeable synthetic peptide NEMO-binding domain peptide (NBD peptide) corresponding to the NEMO amino-terminal alpha-helical region is shown to block TNF-alpha-induced NF-kB activation. The interaction of IKγNEMO with the IKK complex is vital for t | |||
TN1504 | cAMP NF-κB PI3K | ||
Citreorosein is a cAMP phosphodiesterase inhibitor, it has anti-inflammatory effect, inhibits proinflammatory cytokines production through the inhibition of both MAPKs and AKT-mediated IκB kinase (IKK) phosphorylation and subsequent inhibition of transcription factor NF-κB activation. | |||
TN2327 | NOS NF-κB COX | ||
Zedoarondiol has anti-inflammatory activity, inhibits iNOS, COX-2, and pro-inflammatory cytokine expressions by suppressing the phosphorylations of IKK and MAPKs, and by subsequently inactivating the NF-kappaB pathway. | |||
T73470 | |||
PF-184 是一种有效的、选择性的 IKK-2抑制剂 (IC50: 37 nM),选择性优于 rhIKK-1、IKKi, 及 30 多种酪氨酸和丝氨酸/苏氨酸激酶。PF-184 可用于炎症研究,如哮喘和慢性阻塞性肺疾病。 | |||
T36198 | |||
Avenanthramide-C methyl ester is an inhibitor of NF-κB activation that acts by blocking the phosphorylation of IKK and IκB (IC50 ~ 40 μM). Through this mechanism, avenanthramide-C methyl ester dose dependently inhibits the expression and secretion of IL-6, IL-8, and MCP-1 in human aortic endothelial cells. | |||
T75010 | |||
TD1092 是一种泛凋亡抑制蛋白 (IAP) 降解剂,可降解 cIAP1,cIAP2和 XIAP。TD1092 激活细胞凋亡蛋白酶 (apoptosis3/7),并通过促进 IAP 降解,导致癌细胞凋亡 (apoptosis)。同时,TD1092 还能够阻断 TNFα介导的 NF-κB 信号通路,抑制 IKK,IkBα,p65,和 p38 的磷酸化。TD1092 可作为 PROTAC,用于癌症研究。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPJ-01100 | UBE2V1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Ubiquitin-Conjugating Enzyme Variant 1a (UBE2V1) is a member of the Ubiquitin-conjugating (E2) enzyme family. The E2 catalytic core domain of UBE2V1 lacks an active site cysteine residue, rendering it catalytically inactive on its own. However, in the cytoplasm UBE2V1 is able to form a catalytically active complex with UBE2N/Ubc13, which mediates the synthesis Lys63-linked Ubiquitin chains and is required for NF-kappa B activation. UBE2V1 is required for UBE2N (Ubc13)/UBE2V1 Complex-dependent Lys63-linked Ubiquitin chain formation. More specifically, UBE2V1 orients the Ubiquitin molecule to favor linkage at Lys63 via a non-covalent interaction with the Ubiquitin molecule. The UBE2V1-UBE2N heterodimer catalyzes the synthesis of non-canonical poly-ubiquitin chains that are linked through Lys63. This type of poly-ubiquitination activates IKK and does not seem to involve protein degradation by the proteasome. UBE2V1 plays a role in the activation of NF-kappa-B mediated by IL1B, TNF, TRAF6, and TRAF2. It mediates transcriptional activation of target genes. UBE2V1 also controls the progress through the cell cycle and differentiation, the error-free DNA repair pathway and contributes to the survival of cells after DNA damage.
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TMPK-01486 | HLA-A*24:02&B2M&Survivin 2B (AYACNTSTL) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 Cells | ||
Survivin-2B, a known splice variant of survivin, has been reported to promote cell death in some cancer cells, although it keeps prosurvival function in others.survivin-2B promoted autophagy and further regulated cell death by accumulating and stabilizing IKK alpha in the nucleus.
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TMPK-01487 | HLA-A*24:02&B2M&Survivin 2B (AYACNTSTL) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 Cells | ||
Survivin-2B, a known splice variant of survivin, has been reported to promote cell death in some cancer cells, although it keeps prosurvival function in others.survivin-2B promoted autophagy and further regulated cell death by accumulating and stabilizing IKK alpha in the nucleus.
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TMPK-01481 | HLA-A*24:02&B2M&Survivin 2B (AYACNTSTL) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 Cells | ||
Survivin-2B, a known splice variant of survivin, has been reported to promote cell death in some cancer cells, although it keeps prosurvival function in others.survivin-2B promoted autophagy and further regulated cell death by accumulating and stabilizing IKK alpha in the nucleus.
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TMPH-01531 | IKBKB Protein, Human, Recombinant (His) | Human | Baculovirus Insect Cells | ||
Serine kinase that plays an essential role in the NF-kappa-B signaling pathway which is activated by multiple stimuli such as inflammatory cytokines, bacterial or viral products, DNA damages or other cellular stresses. Acts as part of the canonical IKK complex in the conventional pathway of NF-kappa-B activation. Phosphorylates inhibitors of NF-kappa-B on 2 critical serine residues. These modifications allow polyubiquitination of the inhibitors and subsequent degradation by the proteasome. In turn, free NF-kappa-B is translocated into the nucleus and activates the transcription of hundreds of genes involved in immune response, growth control, or protection against apoptosis. In addition to the NF-kappa-B inhibitors, phosphorylates several other components of the signaling pathway including NEMO/IKBKG, NF-kappa-B subunits RELA and NFKB1, as well as IKK-related kinases TBK1 and IKBKE. IKK-related kinase phosphorylations may prevent the overproduction of inflammatory mediators since they exert a negative regulation on canonical IKKs. Phosphorylates FOXO3, mediating the TNF-dependent inactivation of this pro-apoptotic transcription factor. Also phosphorylates other substrates including NCOA3, BCL10 and IRS1. Within the nucleus, acts as an adapter protein for NFKBIA degradation in UV-induced NF-kappa-B activation. Phosphorylates RIPK1 at 'Ser-25' which represses its kinase activity and consequently prevents TNF-mediated RIPK1-dependent cell death. Phosphorylates the C-terminus of IRF5, stimulating IRF5 homodimerization and translocation into the nucleus.
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TMPH-01532 | IKBKB Protein, Human, Recombinant (E. coli, His) | Human | E. coli | ||
Serine kinase that plays an essential role in the NF-kappa-B signaling pathway which is activated by multiple stimuli such as inflammatory cytokines, bacterial or viral products, DNA damages or other cellular stresses. Acts as part of the canonical IKK complex in the conventional pathway of NF-kappa-B activation. Phosphorylates inhibitors of NF-kappa-B on 2 critical serine residues. These modifications allow polyubiquitination of the inhibitors and subsequent degradation by the proteasome. In turn, free NF-kappa-B is translocated into the nucleus and activates the transcription of hundreds of genes involved in immune response, growth control, or protection against apoptosis. In addition to the NF-kappa-B inhibitors, phosphorylates several other components of the signaling pathway including NEMO/IKBKG, NF-kappa-B subunits RELA and NFKB1, as well as IKK-related kinases TBK1 and IKBKE. IKK-related kinase phosphorylations may prevent the overproduction of inflammatory mediators since they exert a negative regulation on canonical IKKs. Phosphorylates FOXO3, mediating the TNF-dependent inactivation of this pro-apoptotic transcription factor. Also phosphorylates other substrates including NCOA3, BCL10 and IRS1. Within the nucleus, acts as an adapter protein for NFKBIA degradation in UV-induced NF-kappa-B activation. Phosphorylates RIPK1 at 'Ser-25' which represses its kinase activity and consequently prevents TNF-mediated RIPK1-dependent cell death. Phosphorylates the C-terminus of IRF5, stimulating IRF5 homodimerization and translocation into the nucleus.
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TMPY-02544 | FANCA Protein, Human, Recombinant (His) | Human | Baculovirus Insect Cells | ||
FANCA is one of the six known Fanconi anemia gene products (FANCA, FANCC, FANCD2, FANCE, FANCF, and FANCG proteins). Fanconi anemia (FA) is a genetic disorder predisposing to aplastic anemia and cancer characterized by hypersensitivity to DNA-damaging agents and oxidative stress. FANCA associates with the IκB kinase (IKK) signalsome via interaction with IKK2. Components of the FANCA complex undergo rapid, stimulus-dependent changes in phosphorylation, which are blocked by kinase-inactive IKK2.
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TMPH-02194 | TAB2 Protein, Human, Recombinant (His & Myc) | Human | Baculovirus Insect Cells | ||
Adapter required to activate the JNK and NF-kappa-B signaling pathways through the specific recognition of 'Lys-63'-linked polyubiquitin chains by its RanBP2-type zinc finger (NZF). Acts as an adapter linking MAP3K7/TAK1 and TRAF6 to 'Lys-63'-linked polyubiquitin chains. The RanBP2-type zinc finger (NZF) specifically recognizes Lys-63'-linked polyubiquitin chains unanchored or anchored to the substrate proteins such as RIPK1/RIP1: this acts as a scaffold to organize a large signaling complex to promote autophosphorylation of MAP3K7/TAK1, and subsequent activation of I-kappa-B-kinase (IKK) core complex by MAP3K7/TAK1. Regulates the IL1-mediated translocation of NCOR1 out of the nucleus. Involved in heart development.
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TMPH-01001 | BCL10 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Plays a key role in both adaptive and innate immune signaling by bridging CARD domain-containing proteins to immune activation. Acts by channeling adaptive and innate immune signaling downstream of CARD domain-containing proteins CARD9, CARD11 and CARD14 to activate NF-kappa-B and MAP kinase p38 (MAPK11, MAPK12, MAPK13 and/or MAPK14) pathways which stimulate expression of genes encoding pro-inflammatory cytokines and chemokines. Recruited by activated CARD domain-containing proteins: homooligomerized CARD domain-containing proteins form a nucleating helical template that recruits BCL10 via CARD-CARD interaction, thereby promoting polymerization of BCL10, subsequent recruitment of MALT1 and formation of a CBM complex. This leads to activation of NF-kappa-B and MAP kinase p38 (MAPK11, MAPK12, MAPK13 and/or MAPK14) pathways which stimulate expression of genes encoding pro-inflammatory cytokines and chemokines. Activated by CARD9 downstream of C-type lectin receptors; CARD9-mediated signals are essential for antifungal immunity. Activated by CARD11 downstream of T-cell receptor (TCR) and B-cell receptor (BCR). Promotes apoptosis, pro-caspase-9 maturation and activation of NF-kappa-B via NIK and IKK.
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TMPH-02521 | PYCARD Protein, Mouse, Recombinant (His & Myc) | Mouse | E. coli | ||
Functions as key mediator in apoptosis and inflammation. Promotes caspase-mediated apoptosis involving predominantly caspase-8 and also caspase-9 in a probable cell type-specific manner. Involved in activation of the mitochondrial apoptotic pathway, promotes caspase-8-dependent proteolytic maturation of BID independently of FADD in certain cell types and also mediates mitochondrial translocation of BAX and activates BAX-dependent apoptosis coupled to activation of caspase-9, -2 and -3. Involved in macrophage pyroptosis, a caspase-1-dependent inflammatory form of cell death and is the major constituent of the ASC pyroptosome which forms upon potassium depletion and rapidly recruits and activates caspase-1. In innate immune response believed to act as an integral adapter in the assembly of the inflammasome which activates caspase-1 leading to processing and secretion of proinflammatory cytokines. The function as activating adapter in different types of inflammasomes is mediated by the pyrin and CARD domains and their homotypic interactions. Required for recruitment of caspase-1 to inflammasomes containing certain pattern recognition receptors, such as NLRP2, NLRP3, AIM2 and probably IFI16. In the NLRP1 and NLRC4 inflammasomes seems not be required but facilitates the processing of procaspase-1. In cooperation with NOD2 involved in an inflammasome activated by bacterial muramyl dipeptide leading to caspase-1 activation. May be involved in DDX58-triggered proinflammatory responses and inflammasome activation. In collaboration with AIM2 which detects cytosolic double-stranded DNA may also be involved in a caspase-1-independent cell death that involves caspase-8. In adaptive immunity may be involved in maturation of dendritic cells to stimulate T-cell immunity and in cytoskeletal rearrangements coupled to chemotaxis and antigen uptake may be involved in post-transcriptional regulation of the guanine nucleotide exchange factor DOCK2; the latter function is proposed to involve the nuclear form. Also involved in transcriptional activation of cytokines and chemokines independent of the inflammasome; this function may involve AP-1, NF-kappa-B, MAPK and caspase-8 signaling pathways. For regulation of NF-kappa-B activating and inhibiting functions have been reported. Modulates NF-kappa-B induction at the level of the IKK complex by inhibiting kinase activity of CHUK and IKBK. Proposed to compete with RIPK2 for association with CASP1 thereby down-regulating CASP1-mediated RIPK2-dependent NF-kappa-B activation and activating interleukin-1 beta processing. Modulates host resistance to DNA virus infection, probably by inducing the cleavage of and inactivating CGAS in presence of cytoplasmic double-stranded DNA.
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