TTK (Ab-676) Antibody

說明書

中文名稱：

TTK (Ab-676)兔多克隆抗體
貨號：

CSB-PA586001
規格：

￥2024
圖片：
Immunohistochemistry analysis of paraffin-embedded human brain tissue using TTK (Ab-676) antibody.

Western blot analysis of extracts from HUVEC cells, treated with etoposide (25uM, 24hours), using TTK (Ab-676) antibody.

Western blot analysis of extracts from colo cells (Lane 2), using TTK (Ab-676) antiobdy. The lane on the left is treated with synthesized peptide.
其他：

產品詳情
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靶點詳情

產品詳情

產品名稱：

Rabbit anti-Homo sapiens (Human) TTK Polyclonal antibody
Uniprot No.：

P33981
基因名：

TTK
宿主：

Rabbit
反應種屬：

Human,Mouse
免疫原：

Synthesized non-phosphopeptide derived from Human TTK around the phosphorylation site of threonine 676 (D-T-T(p)-S-V).
免疫原種屬：

Homo sapiens (Human)
克隆類型：

Polyclonal
純化方式：

The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
濃度：

It differs from different batches. Please contact us to confirm it.
產品提供形式：

Liquid
應用范圍：

ELISA,WB,IHC

推薦稀釋比：

Application	Recommended Dilution
WB	1:500-1:3000
IHC	1:50-1:100

Protocols：

ELISA Protocol
Western Blotting (WB) Protocol
Immunohistochemistry (IHC) Protocol
儲存條件：

Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
貨期：

Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
用途：

For Research Use Only. Not for use in diagnostic or therapeutic procedures.

產品評價

靶點詳情

功能：

Phosphorylates proteins on serine, threonine, and tyrosine. Probably associated with cell proliferation. Phosphorylates MAD1L1 to promote mitotic checkpoint signaling. Essential for chromosome alignment by enhancing AURKB activity (via direct CDCA8 phosphorylation) at the centromere, and for the mitotic checkpoint.
基因功能參考文獻：
1. Treatment of a xenograft model of a CTNNB1-mutant cell line with the TTK inhibitor NTRC 0066-0 resulted in complete inhibition of tumor growth. Mutations in CTNNB1 occur at relatively high frequency in endometrial cancer and hepatocellular carcinoma, which are known to express high TTK levels. We propose mutant CTNNB1 as a prognostic drug response biomarker, enabling the selection of patients most likely to respond to TTK PMID: 28751540
2. Following lentiviral shRNA knockdown in several human liver cancer cell lines, we demonstrated that TTK boosts cell growth and promotes cell spreading; as well as protects against senescence and decreases autophagy. In an experimental animal model, we show that in vitro knockdown of TTK effectively blocks intrahepatic growth of human HCC xenografts. PMID: 27618777
3. The expression of TTK in gallbladder cancer (GBC) is lower than that in normal tissues. Higher levels of TTK expression in GBC are concomitant with longer overall survival. PMID: 28883705
4. TTK is a favorable prognostic biomarker associated with triple-negative breast cancer survival. PMID: 27833085
5. Therefore, Mps1 promotes checkpoint activation through sequentially phosphorylating Knl1, Bub1, and Mad1. This sequential multi-target phosphorylation cascade makes the checkpoint highly responsive to Mps1 and to kinetochore-microtubule attachment. PMID: 28072388
6. Both monopolar spindle 1 (MPS1) and miR-21 depletion suppressed glioblastoma (GBM) cell proliferation, whereas, ectopic expression of miR-21 rescued GBM cell growth from MPS1 inhibition. PMID: 25991676
7. The TTK gene on 6q14.1 encodes a dual-specificity protein kinase (hMps1), a key spindle assembly checkpoint protein that regulates the proper chromosomal alignment and segregation during mitosis. PMID: 28777004
8. Data show that Thr/Tyr kinase (TTK)/monopolar spindle 1 kinase (Mps-1) is overexpressed in malignant mesothelioma (MM) and that its expression correlates with poor patients' outcome. PMID: 28759042
9. Separate elements in the Mps1 N-terminal extension and tetratricopeptide repeat domains govern localization to either the kinetochore or the centrosome. PMID: 27339139
10. inhibition of the novel mitochondrial function Mps1 is sufficient to kill tumor cells. PMID: 27383047
11. Data suggest that point mutations in the catalytic domain of MPS1 (C604Y and C604W) give rise to enzymes that retain catalytic activity but are resistant to protein kinase inhibitors; these studies investigated crystal structures of recombinant wild-type and mutant MPS1 with various protein kinase inhibitors bound to ATP-binding pocket of catalytic domain. PMID: 28726638
12. critical role in preventing aneuploidy-induced cell death in pancreatic cancer PMID: 28380042
13. HLF-mediated miR-132 directly suppresses TTK expression, thus exerting inhibitory effects on cancer cell proliferation, metastasis and radioresistance. PMID: 27522003
14. Mps1 is sumoylated and that plays an essential role in regulating Mps1 functions during mitosis. PMID: 26675261
15. Results suggest that monopolar spindle 1 kinase (MPS1) inhibition could be used as a therapeutic strategy for targeting tetraploid cancer cells. PMID: 26637805
16. Cetn3 inhibits Mps1 autophosphorylation at Thr-676, a known site of T-loop autoactivation, and interferes with Mps1-dependent phosphorylation of Cetn2. The cellular overexpression of Cetn3 attenuates the incorporation of Cetn2 into centrioles and centrosome reduplication, whereas depletion of Cetn3 generates extra centrioles. PMID: 26354417
17. Knockdown of Cdkn3 stabilizes Mps1 at centrosomes. PMID: 26586430
18. TTK contributes to hepatocellular carcinoma tumorigenesis via promoting cell proliferation and migration PMID: 26418879
19. Interaction of the central domain of ARHGEF17 with Mps1. PMID: 26953350
20. Data show that TTK protein kinase (hMps1) interacts with proto-oncogene protein MDM2 in vivo and in vitro. PMID: 26531827
21. Depletion of Mps1 reduces tumor cell viability relative to normal cells. PMID: 26398286
22. Mps1 functions in chromosome alignment by orchestrating Ndc80C-MT interactions PMID: 26240331
23. High Mps1 expression, both at mRNA and protein levels, was found to be associated with high tumor grade, high Ki67 expression, and worse survival ,particularly in Triple Negative Breast Cancer . PMID: 25731686
24. Daata show five point mutations in the kinase domain of mitotic checkpoint kinase MPS1 that confer resistance against multiple inhibitors. PMID: 26202014
25. N-terminal of Mps1 was identified a high sequence similarity to the classic NES,a fusion of this motif with EGFP results in dramatic exclusion of the fusion protein from the nucleus. PMID: 25886724
26. TTK was up-regulated in HCC specimens. TTK overexpression promoted cell proliferation, anchor-dependent colony formation and resistance to sorafenib of HCC cells. PMID: 24905462
27. The dual-specificity protein kinase TTK, which is a key mitotic checkpoint regulator with links to p53 signaling, was further shown to be a promising overall prognostic marker for Hepatocellular carcinoma in the large patient cohort. PMID: 24859455
28. the checkpoint protein kinase monopolar spindle 1 (Mps1) directly bound to Ndc80C through two independent interactions. PMID: 26068854
29. the amino-terminal localization module of the spindle assembly checkpoint protein kinase MPS1 directly interacts with the HEC1 (highly expressed in cancer 1) calponin homology domain in the NDC80 (nuclear division cycle 80) kinetochore complex in vitro, in a phosphorylationdependent manner. PMID: 26068855
30. results highlight the importance of dynamic autophosphorylation of Mps1 in regulating accurate chromosome segregation and ensuring proper mitotic progression PMID: 25265012
31. Data suggest that MPS1 kinase inhibition as a pancreatic ductal adenocarcinoma (PDAC) treatment strategy. PMID: 24282275
32. High TTK protein expression is associated with pancreatic cancer. PMID: 25137017
33. PP2A-B56 is a key phosphatase for the removal of the Mps1-mediated Knl1 phosphorylations necessary for Bub1/BubR1 recruitment in mammalian cells. PMID: 25246613
34. findings suggest that high levels of Mps1 contribute to tumorigenesis by attenuating the spindle assembly checkpoint PMID: 25063032
35. Our results provide evidence of a newly identified hMps1 phosphorylation site that is involved in the mitotic checkpoint and that CHK2 contributes to chromosomal stability through hMps1. PMID: 24764296
36. Mps1 governs chromosomal organization during the early stage of mitosis to facilitate proper chromosome segregation. PMID: 24934155
37. MPS1 inhibitors may exert robust anticancer activity, either as standalone therapeutic interventions or combined with microtubule-targeting chemicals. PMID: 23933817
38. Data show that TTK protein kinase, lymphocyte antigen 6 complex locus K and insulin-like growth factor (IGF)-II mRNA binding protein 3 are tumor-associated antigens recognized by cytotoxic T lymphocytes and HLA-A24-restricted epitope peptides. PMID: 17784873
39. sustained MPS1 activity is required for maintaining both the MAD1.C-MAD2 complex and open MAD2 (O-MAD2) at unattached kinetochores to facilitate C-MAD2 production PMID: 24151075
40. a novel role for Aurora B-Hec1-Mps1 signaling axis in governing accurate chromosome segregation in mitosis PMID: 24187132
41. two proteins that interact with BLM, RMI1 and RMI2, are phosphorylated upon SAC activation, and, like BLM, RMI1, and RMI2, are phosphorylated in an MPS1-dependent manner. PMID: 24108125
42. MPS1 is protein kinase overexpressed in triple-negative breast cancer. PMID: 23700430
43. Mps1 is an acidophilic kinase with a striking tendency for phosphorylation of threonines. PMID: 23510141
44. Ultraviolet-C irradiation delays mitotic progression by recruiting Mps1 to kinetochores. PMID: 23531678
45. Data propose that Chk1 and Mps1 jointly regulate Aurora-B, MCAK, Kif2b and Hec1 to correct merotelic attachments. These results suggest a role for Chk1 and Mps1 in error correction. PMID: 23321637
46. Oncogenic B-Raf(V600E) abrogates the AKT/B-Raf/Mps1 interaction in melanoma cells. PMID: 23726842
47. a VDAC3-Mps1 module at the centrosome promotes ciliary disassembly during cell cycle entry. PMID: 23388454
48. Mps1 stimulates Aurora B recruitment to centromere. PMID: 22732840
49. These data are consistent with a model in which Aurora B activity relieves a tetratricopeptide repeat domain-dependent inhibitory constraint on MPS1 localization. PMID: 23569217
50. We propose that , and that persistent phosphorylation of Mps1 through BRAF(V600E) signaling is a key event in disrupting the control of centrosome duplication and chromosome stability that may contribute to tumorigenesis. PMID: 22430208
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蛋白家族：

Protein kinase superfamily, Ser/Thr protein kinase family
組織特異性：

Present in rapidly proliferating cell lines.
數據庫鏈接：

HGNC: 12401

OMIM: 604092

KEGG: hsa:7272

STRING: 9606.ENSP00000358813

UniGene: Hs.169840

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