目录号 | 产品详情 | 靶点 | |
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T6363 | IRE1 | ||
4μ8C (IRE1 Inhibitor III) 是一种有效且特异性的 IRE1α 抑制剂。 | |||
T9564 | IRE1 | ||
IRE1α kinase-IN-1 是IRE1α 的选择性抑制剂(IC50为 77 nM),对 IRE1α 的选择性高于 IRE1β 亚型 100 倍。它抑制内质网诱导的 IRE1α 寡聚和自磷酸化,并抑制 IRE1α RNase 活性 (IC50=80 nM)。 | |||
TQ0076 | IRE1 | ||
KIRA6 是一种 IRE1α RNase 激酶的有效抑制剂,IC50为0.6 µM。它可以触发细胞凋亡反应。 | |||
TQ0101 | IRE1 | ||
MKC3946 是一种有效的可溶性 IRE1α 抑制剂,可在多发性骨髓瘤细胞系中引发适度的生长抑制,可用于癌症研究。 | |||
T3654 | IRE1 | ||
APY29 是 IRE1α 的变构调节剂;抑制 IRE1α 自磷酸化,IC50值为 280 nM,并激活 IRE1α RNase 活性。 | |||
T12071 | IRE1 | ||
MKC9989 是一种羟基芳基醛 (HAA) 的抑制剂,抑制 IRE1α的 IC50值在 0.23 到 44 μM 之间。 | |||
T6681 | IRE1 | ||
STF-083010 是一种 IRE1α 核酸内切酶的选择性抑制剂。 | |||
T15594 | IRE1 | ||
MKC8866 是一种选择性IRE1 RNase 抑制剂,在体外的IC50为 0.29 μM,是水杨醛类似物。 它抑制乳腺癌细胞中的 IRE1 RNase,导致促肿瘤因子的产生减少,并且可以抑制前列腺癌 (PCa) 肿瘤的生长。它强烈抑制二硫苏糖醇诱导的 XBP1s 表达,EC50为 0.52 μM。 | |||
T11488 | IRE1 | ||
GSK2850163 是新型的肌醇需要酶-1α (IRE1α) 抑制剂,抑制 IRE1α 激酶活性的 IC50为 20nM,对 RNA 酶活性也有抑制活性,IC50为200 nM。 | |||
T11762L | IRE1 | ||
Kira8 (AMG-18) 是一种单选择性 IRE1α 抑制剂,可变构减弱 IRE1α RNase 活性,IC50为 5.9 nM。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-04753 | IRE1 Protein, Human, Recombinant (aa 465-977) | Human | Baculovirus-Insect Cells | ||
Endoplasmic reticulum stress and hypoxia are necessary components of malignant tumors growth and suppression of ERN1 (from endoplasmic reticulum to nuclei-1) signalling pathway, which is linked to the apoptosis and cell death processes, significantly decreases proliferative processes. An enhanced expression of TP53 gene in ERN1 knockdown glioma cells correlates with the decreased level of ubiquitin ligase MDM2 and increased expression level of USP7 which deubiquitinates TP53 and MDM2 and induces TP53-dependent cell growth repression and apoptosis. Thus, the expression of genes encoding TP53 and related to TP53 factors depends upon the endoplasmic reticulum stress signaling as well as on hypoxia, and correlates with suppression of glioma growth under ERN1 knockdown. The dependence of insulin-like growth binding proteins as well as IGF2BP3 and HTRA1 gene expressions in U87 glioma cells on ERN1 signaling enzyme function and hypoxia, indicating its participation in the regulation of metabolic and proliferative processes via IGF/INS receptors, because endoplasmic reticulum stress is an important component of tumor growth and metabolic diseases.
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TMPY-04413 | IRE1 Protein, Human, Recombinant (aa 465-977, His & GST) | Human | Baculovirus-Insect Cells | ||
Endoplasmic reticulum stress and hypoxia are necessary components of malignant tumors growth and suppression of ERN1 (from endoplasmic reticulum to nuclei-1) signalling pathway, which is linked to the apoptosis and cell death processes, significantly decreases proliferative processes. An enhanced expression of TP53 gene in ERN1 knockdown glioma cells correlates with the decreased level of ubiquitin ligase MDM2 and increased expression level of USP7 which deubiquitinates TP53 and MDM2 and induces TP53-dependent cell growth repression and apoptosis. Thus, the expression of genes encoding TP53 and related to TP53 factors depends upon the endoplasmic reticulum stress signaling as well as on hypoxia, and correlates with suppression of glioma growth under ERN1 knockdown. The dependence of insulin-like growth binding proteins as well as IGF2BP3 and HTRA1 gene expressions in U87 glioma cells on ERN1 signaling enzyme function and hypoxia, indicating its participation in the regulation of metabolic and proliferative processes via IGF/INS receptors, because endoplasmic reticulum stress is an important component of tumor growth and metabolic diseases.
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TMPH-02639 | HSPA5 Protein, Mouse, Recombinant (His) | Mouse | Yeast | ||
Endoplasmic reticulum chaperone that plays a key role in protein folding and quality control in the endoplasmic reticulum lumen. Involved in the correct folding of proteins and degradation of misfolded proteins via its interaction with DNAJC10/ERdj5, probably to facilitate the release of DNAJC10/ERdj5 from its substrate. Acts as a key repressor of the ERN1/IRE1-mediated unfolded protein response (UPR). In the unstressed endoplasmic reticulum, recruited by DNAJB9/ERdj4 to the luminal region of ERN1/IRE1, leading to disrupt the dimerization of ERN1/IRE1, thereby inactivating ERN1/IRE1. Accumulation of misfolded protein in the endoplasmic reticulum causes release of HSPA5/BiP from ERN1/IRE1, allowing homodimerization and subsequent activation of ERN1/IRE1. Plays an auxiliary role in post-translational transport of small presecretory proteins across endoplasmic reticulum (ER). May function as an allosteric modulator for SEC61 channel-forming translocon complex, likely cooperating with SEC62 to enable the productive insertion of these precursors into SEC61 channel. Appears to specifically regulate translocation of precursors having inhibitory residues in their mature region that weaken channel gating. May also play a role in apoptosis and cell proliferation.
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TMPH-02638 | HSPA5 Protein, Mouse, Recombinant (E. coli, His) | Mouse | E. coli | ||
Endoplasmic reticulum chaperone that plays a key role in protein folding and quality control in the endoplasmic reticulum lumen. Involved in the correct folding of proteins and degradation of misfolded proteins via its interaction with DNAJC10/ERdj5, probably to facilitate the release of DNAJC10/ERdj5 from its substrate. Acts as a key repressor of the ERN1/IRE1-mediated unfolded protein response (UPR). In the unstressed endoplasmic reticulum, recruited by DNAJB9/ERdj4 to the luminal region of ERN1/IRE1, leading to disrupt the dimerization of ERN1/IRE1, thereby inactivating ERN1/IRE1. Accumulation of misfolded protein in the endoplasmic reticulum causes release of HSPA5/BiP from ERN1/IRE1, allowing homodimerization and subsequent activation of ERN1/IRE1. Plays an auxiliary role in post-translational transport of small presecretory proteins across endoplasmic reticulum (ER). May function as an allosteric modulator for SEC61 channel-forming translocon complex, likely cooperating with SEC62 to enable the productive insertion of these precursors into SEC61 channel. Appears to specifically regulate translocation of precursors having inhibitory residues in their mature region that weaken channel gating. May also play a role in apoptosis and cell proliferation.
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