目录号 | 产品详情 | 靶点 | |
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TQ0003 | PI3K Autophagy | ||
740 Y-P (740YPDGFR) 是一个细胞渗透性PI3K 激活剂。它能结合含有 p85 的 N- 和 C- 末端 SH2 结构域的 GST 融合蛋白。 | |||
T13475 | Others Endogenous Metabolite | ||
β-Aminopropionitrile (3-Aminopropionitrile) 是赖氨酰氧化酶的特异性抑制剂。 | |||
T1912 | Apoptosis CDK | ||
Dinaciclib (SCH 727965) 是一种 CDK 抑制剂,抑制 CDK1、CDK2、CDK5 和 CDK9 (IC50分=3/1/1/4 nM),具有选择性。Dinaciclib 具有潜在的抗肿瘤活性,可以抑制胸甘 (dThd) DNA 的整合。 | |||
T2503 | Apoptosis Caspase Autophagy | ||
PAC-1 (Procaspase activating compound 1) 是一种 procaspase-3激活剂,诱导癌细胞凋亡,EC50为 2.08 μM,可用于研究淋巴瘤、黑色素瘤、实体瘤、乳腺癌和胸癌等治疗的试验。 | |||
TP2106L | Neurotensin Receptor | ||
Urantide acetate(669089-53-6 free base) 是一种选择性和竞争性的 urotensin-II (UT) 受体拮抗剂 (pKB = 8.3)。体外阻断 hU-II 诱导的胸主动脉收缩。对去甲肾上腺素或内皮素 1 诱导的收缩或乙酰胆碱诱导的松弛没有影响。在钙动员测定(在表达 hUT 受体的 CHO 细胞中)中表现为部分激动剂。 | |||
T5S1889 | Others | ||
Yunaconitine (Guayewuanine B) 是一种乌头类生物碱,具有剧毒。 | |||
TN1724 | P450 Antioxidant | ||
Harmalol hydrochloride (Harmidol hydrochloride) 是一种可从Peganum harmala L.的种子中提取出来的β-咔啉生物碱。Harmalol hydrochloride 是Harmaline 的主要代谢产物,在转录和翻译后水平上显著抑制二恶英介导的 CYP1A1 诱导。Harmalol hydrochloride 在去氧肾上腺素或KCl 预先收缩的分离大鼠胸主动脉制剂中显示出血管松弛活性。 Harmalol hydrochloride 具有抗氧化活性. | |||
T20692 | |||
Schistoflrfamide is a locust myosuppressin, it is isolated from the thoracic nervous system of the locust Schistocerca gregaria. | |||
TP2106 | |||
Selective and competitive urotensin-II (UT) receptor antagonist (pKB = 8.3). Blocks hU-II induced contractions in thoracic aorta ex vivo. Exhibits no effect on noradrenaline or endothelin 1-induced contraction or on acetylcholine-induced relaxation. Behav | |||
T83596 | |||
(+)-Osbeckic acid,一种Tartary Buckwheat中提取的血管松弛剂,对Sprague-Dawley大鼠胸主动脉环展现出显著的血管舒张效应,其半数有效浓度(EC50)为887 μM。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-03052 | MFAP5 Protein, Human, Recombinant (His) | Human | HEK293 | ||
MFAP5 (Microfibril Associated Protein 5, also known as MAGP2) is a Protein Coding gene. MFAP5 is a component of the elastin-associated microfibrils. It belongs to the MFAP family. As a 25-kD microfibril-associated glycoprotein, MFAP5 is rich in serine and threonine residues. It stimulates the assembly of elastic fibers, a complex structure composed of a tropoelastin inner core and microfibril outer mantle comprising proteins such as fibrillins and microfibril-associated glycoproteins that guide tropoelastin deposition. MFAP5 also stabilizes type 1 procollagen and thus plays an important role in extracellular matrix homeostasis. It has multiple binding regions on fibrillins and has a covalent periodic association with fibrillin-containing microfibrils. Diseases associated with MFAP5 include Aortic Aneurysm, Familial Thoracic 9, and Familial Thoracic Aortic Aneurysm And Aortic Dissection.
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TMPY-01358 | ALK-5 Protein, Human, Recombinant (His & hFc) | Human | HEK293 | ||
Transforming growth factor, beta receptor I, also known as Transforming growth factor-beta receptor type I , Serine / threonine-protein kinase receptor R4, Activin receptor-like kinase 5, SKR4, ALK-5, and TGFBR1, is a single-pass type I membrane protein that belongs to the protein kinase superfamily and TGFB receptor subfamily. TGFBR1 / ALK-5 is found in all tissues examined. It is most abundant in placenta and least abundant in brain and heart. TGF-beta functions as a tumor suppressor by inhibiting the cell cycle in the G1 phase. Administration of TGF-beta is able to protect against mammary tumor development in transgenic mouse models in vivo. Disruption of the TGF-beta/SMAD pathway has been implicated in a variety of human cancers, with the majority of colon and gastric cancers being caused by an inactivating mutation of TGF-beta RII. On ligand binding, TGFBR1 / ALK-5 forms a receptor complex consisting of two type I I and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which auto-phosphorylate, then bind and activate SMAD transcriptional regulators. TGF-beta signaling via TGFBR1 / ALK-5 is not required in myocardial cells during mammalian cardiac development, but plays an irreplaceable cell-autonomous role regulating cellular communication, differentiation and proliferation in endocardial and epicardial cells. Defects in TGFBR1 / ALK-5 are the cause of Loeys-Dietz syndrome type 1A (LDS1A), Loeys-Dietz syndrome type 2A (LDS2A), and aortic aneurysm familial thoracic type 5 (AAT5).
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TMPY-05771 | ALK-5 Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Transforming growth factor, beta receptor I, also known as Transforming growth factor-beta receptor type I , Serine / threonine-protein kinase receptor R4, Activin receptor-like kinase 5, SKR4, ALK-5, and TGFBR1, is a single-pass type I membrane protein that belongs to the protein kinase superfamily and TGFB receptor subfamily. TGFBR1 / ALK-5 is found in all tissues examined. It is most abundant in placenta and least abundant in brain and heart. TGF-beta functions as a tumor suppressor by inhibiting the cell cycle in the G1 phase. Administration of TGF-beta is able to protect against mammary tumor development in transgenic mouse models in vivo. Disruption of the TGF-beta/SMAD pathway has been implicated in a variety of human cancers, with the majority of colon and gastric cancers being caused by an inactivating mutation of TGF-beta RII. On ligand binding, TGFBR1 / ALK-5 forms a receptor complex consisting of two type I I and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which auto-phosphorylate, then bind and activate SMAD transcriptional regulators. TGF-beta signaling via TGFBR1 / ALK-5 is not required in myocardial cells during mammalian cardiac development, but plays an irreplaceable cell-autonomous role regulating cellular communication, differentiation and proliferation in endocardial and epicardial cells. Defects in TGFBR1 / ALK-5 are the cause of Loeys-Dietz syndrome type 1A (LDS1A), Loeys-Dietz syndrome type 2A (LDS2A), and aortic aneurysm familial thoracic type 5 (AAT5).
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TMPY-04366 | ALK-5 Protein, Human, Recombinant (aa 200-503, His & GST) | Human | Baculovirus-Insect Cells | ||
Transforming growth factor, beta receptor I, also known as Transforming growth factor-beta receptor type I , Serine / threonine-protein kinase receptor R4, Activin receptor-like kinase 5, SKR4, ALK-5, and TGFBR1, is a single-pass type I membrane protein that belongs to the protein kinase superfamily and TGFB receptor subfamily. TGFBR1 / ALK-5 is found in all tissues examined. It is most abundant in placenta and least abundant in brain and heart. TGF-beta functions as a tumor suppressor by inhibiting the cell cycle in the G1 phase. Administration of TGF-beta is able to protect against mammary tumor development in transgenic mouse models in vivo. Disruption of the TGF-beta/SMAD pathway has been implicated in a variety of human cancers, with the majority of colon and gastric cancers being caused by an inactivating mutation of TGF-beta RII. On ligand binding, TGFBR1 / ALK-5 forms a receptor complex consisting of two type I I and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which auto-phosphorylate, then bind and activate SMAD transcriptional regulators. TGF-beta signaling via TGFBR1 / ALK-5 is not required in myocardial cells during mammalian cardiac development, but plays an irreplaceable cell-autonomous role regulating cellular communication, differentiation and proliferation in endocardial and epicardial cells. Defects in TGFBR1 / ALK-5 are the cause of Loeys-Dietz syndrome type 1A (LDS1A), Loeys-Dietz syndrome type 2A (LDS2A), and aortic aneurysm familial thoracic type 5 (AAT5).
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