目录号 | 产品详情 | 靶点 | |
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T11110 | DUB | ||
DUB-IN-1 是一种泛素特异性蛋白酶 (USP) 的活性抑制剂,对 USP8 的IC50值为 0.24 μM。 | |||
T36682 | DUB | ||
USP30 inhibitor 18 是有效的USP30选择性抑制剂,IC50为 0.02 μM。它增加蛋白质泛素化并加速线粒体自噬。 | |||
T9122 | DUB | ||
XL177A 是一种选择性不可逆的 USP7 抑制剂,IC50为 0.34 nM。它通过 p53 依赖性机制引发癌杀伤细胞作用。 | |||
T11112 | DUB | ||
DUB-IN-3 是强效去泛素酶 (USP) 酶抑制剂,对 USP8 的 IC50值为 0.56 μM。 | |||
T11111 | DUB | ||
DUB-IN-2 是一种有效的去泛素酶抑制剂,能够抑制 USP8 的活性,IC50值为 0.28 μM。 | |||
T11209 | DUB | ||
EOAI3402143 是一种去泛素化酶抑制剂,以剂量依赖性抑制 Usp9x/Usp24和 Usp5,增加肿瘤细胞凋亡。 | |||
T15604 | DUB | ||
IU1-47 是一种特异性 USP14抑制剂,IC50为 0.6 μM。它诱导培养的神经元中 tau 蛋白降解。它抑制 IsoT/USP5, IC50为 20 μM。 | |||
T5461 | DUB | ||
GNE 6640 是一种选择性泛素特异性肽酶 7(USP7)的非共价抑制剂,其对全长USP7、USP7 催化结构域、全长USP43 以及 Ub-MDM2 的IC50值分别为 0.75 μM、0.43 μM、20.3 μM 和 0.23 μM。 | |||
T1757 | DUB | ||
ML323 是一种有效的可逆的USP1-UAF1抑制剂,在Ub-Rho 测定实验中,IC50为 76 nM。在使用 K63 连接的双泛素 (di-Ub) 和单泛素化 PCNA 的正交凝胶测定中(Ub-PCNA)分别作为底物。 | |||
T13268 | DUB | ||
USP7-IN-1 是泛素蛋白特异性蛋白酶的选择性、可逆性抑制剂,IC50为 77 μM,可用于癌症研究。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-02522 | OTUB2 Protein, Human, Recombinant (His) | Human | E. coli | ||
Otubain 2 (OTUB2) is a member of DUBs that belong to the ovarian tumour (OTU) superfamily of proteins which consists of a five-stranded β-sheet sandwiched in between a small helical amino-terminal region consisting of α1 and α2, and a large helical region comprised of α3-α10. Like other DUBs, otubain 2 (OTUB2) cleaves proteins precisely at the ubiquitin-protein bond so that ubiquitylation process can be reversed and regulated. Otubain 2 (OTUB2)'s active-site cleft is sterically occluded by a novel loop conformation resulting in an oxyanion hole, which consists uniquely of backbone amides. Furthermore, the residues that orient and stabilize the active-site histidine of otubain 2 (OTUB2) are different from other cysteine proteases. This reorganization of the active-site topology provides a possible explanation for the low turnover and substrate specificity of the otubains.
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TMPY-02214 | OTUB1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Ubiquitin thioesterase OTUB1, also known as Deubiquitinating enzyme OTUB1, OTU domain-containing ubiquitin aldehyde-binding protein 1, Otubain-1, Ubiquitin-specific-processing protease OTUB1, OTUB1 and OTB1, is a cytoplasm protein that belongs to the peptidase C65 family. OTUB1 is a hydrolase that can remove conjugated ubiquitin from proteins and plays an important regulatory role at the level of protein turnover by preventing degradation. OTUB1 is a regulator of T-cell anergy, a phenomenon that occurs when T-cells are rendered unresponsive to antigen rechallenge and no longer respond to their cognate antigen. OTUB1 acts via its interaction with RNF128 / GRAIL, a crucial inductor of CD4 T-cell anergy. Isoform 1 of OTUB1 destabilizes RNF128, leading to prevent anergy. In contrast, isoform 2 of OTUB1 stabilizes RNF128 and promotes anergy. OTUB1 regulates RNF128-mediated ubiquitination, but does not deubiquitinate polyubiquitinated RNF128. Deubiquitinates estrogen receptor alpha (ESR1). OTUB1 mediates deubiquitination of 'Lys-48'-linked polyubiquitin chains, but not 'Lys-63'-linked polyubiquitin chains. OTUB1 is also capable of removing NEDD8 from NEDD8 conjugates, but with a much lower preference compared to 'Lys-48'-linked ubiquitin.
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TMPH-01621 | BRCC3 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Metalloprotease that specifically cleaves 'Lys-63'-linked polyubiquitin chains. Does not have activity toward 'Lys-48'-linked polyubiquitin chains. Component of the BRCA1-A complex, a complex that specifically recognizes 'Lys-63'-linked ubiquitinated histones H2A and H2AX at DNA lesions sites, leading to target the BRCA1-BARD1 heterodimer to sites of DNA damage at double-strand breaks (DSBs). In the BRCA1-A complex, it specifically removes 'Lys-63'-linked ubiquitin on histones H2A and H2AX, antagonizing the RNF8-dependent ubiquitination at double-strand breaks (DSBs). Catalytic subunit of the BRISC complex, a multiprotein complex that specifically cleaves 'Lys-63'-linked ubiquitin in various substrates. Mediates the specific 'Lys-63'-specific deubiquitination associated with the COP9 signalosome complex (CSN), via the interaction of the BRISC complex with the CSN complex. The BRISC complex is required for normal mitotic spindle assembly and microtubule attachment to kinetochores via its role in deubiquitinating NUMA1. Plays a role in interferon signaling via its role in the deubiquitination of the interferon receptor IFNAR1; deubiquitination increases IFNAR1 activity by enhancing its stability and cell surface expression. Down-regulates the response to bacterial lipopolysaccharide (LPS) via its role in IFNAR1 deubiquitination.
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TMPH-02285 | USP6 Protein, Human, Recombinant (His & KSI) | Human | E. coli | ||
Deubiquitinase with an ATP-independent isopeptidase activity, cleaving at the C-terminus of the ubiquitin moiety. Catalyzes its own deubiquitination. In vitro, isoform 2, but not isoform 3, shows deubiquitinating activity. Promotes plasma membrane localization of ARF6 and selectively regulates ARF6-dependent endocytic protein trafficking. Is able to initiate tumorigenesis by inducing the production of matrix metalloproteinases following NF-kappa-B activation.
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TMPH-02640 | ZC3H12A Protein, Mouse, Recombinant (His & Myc) | Mouse | E. coli | ||
Endoribonuclease involved in various biological functions such as cellular inflammatory response and immune homeostasis, glial differentiation of neuroprogenitor cells, cell death of cardiomyocytes, adipogenesis and angiogenesis. Functions as an endoribonuclease involved in mRNA decay. Modulates the inflammatory response by promoting the degradation of a set of translationally active cytokine-induced inflammation-related mRNAs, such as IL6 and IL12B, during the early phase of inflammation. Prevents aberrant T-cell-mediated immune reaction by degradation of multiple mRNAs controlling T-cell activation, such as those encoding cytokines (IL6 and IL2), cell surface receptors (ICOS, TNFRSF4 and TNFR2) and transcription factor (REL). Inhibits cooperatively with ZC3H12A the differentiation of helper T cells Th17 in lungs. They repress target mRNA encoding the Th17 cell-promoting factors IL6, ICOS, REL, IRF4, NFKBID and NFKBIZ. The cooperation requires RNA-binding by RC3H1 and the nuclease activity of ZC3H12A. Together with RC3H1, destabilizes TNFRSF4/OX40 mRNA by binding to the conserved stem loop structure in its 3'UTR. Self regulates by destabilizing its own mRNA. Cleaves mRNA harboring a stem-loop (SL), often located in their 3'-UTRs, during the early phase of inflammation in a helicase UPF1-dependent manner. Plays a role in the inhibition of microRNAs (miRNAs) biogenesis. Cleaves the terminal loop of a set of precursor miRNAs (pre-miRNAs) important for the regulation of the inflammatory response leading to their degradation, and thus preventing the biosynthesis of mature miRNAs. Plays also a role in promoting angiogenesis in response to inflammatory cytokines by inhibiting the production of antiangiogenic microRNAs via its anti-dicer RNase activity. Affects the overall ubiquitination of cellular proteins. Positively regulates deubiquitinase activity promoting the cleavage at 'Lys-48'- and 'Lys-63'-linked polyubiquitin chains on TNF receptor-associated factors (TRAFs), preventing JNK and NF-kappa-B signaling pathway activation, and hence negatively regulating macrophage-mediated inflammatory response and immune homeostasis. Induces also deubiquitination of the transcription factor HIF1A, probably leading to its stabilization and nuclear import, thereby positively regulating the expression of proangiogenic HIF1A-targeted genes. Involved in a TANK-dependent negative feedback response to attenuate NF-kappaB activation through the deubiquitination of IKBKG or TRAF6 in response to interleukin-1-beta (IL1B) stimulation or upon DNA damage. Prevents stress granules (SGs) formation and promotes macrophage apoptosis under stress conditions, including arsenite-induced oxidative stress, heat shock, and energy deprivation. Plays a role in the regulation of macrophage polarization; promotes IL4-induced polarization of macrophages M1 into anti-inflammatory M2 state. May also act as a transcription factor that regulates the expression of multiple genes involved in inflammatory response, angiogenesis, adipogenesis and apoptosis. Functions as a positive regulator of glial differentiation of neuroprogenitor cells through an amyloid precursor protein (APP)-dependent signaling pathway. Attenuates septic myocardial contractile dysfunction in response to lipopolysaccharide (LPS) by reducing I-kappa-B-kinase (IKK)-mediated NF-kappa-B activation, and hence myocardial proinflammatory cytokine production.
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