NPM (Phospho-Thr234) ELISA Kit

Name: NPM (Phospho-Thr234) ELISA Kit
SKU: DEIA-XYA1341
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

cultured cells

Species Reactivity

Human; Mouse; Rat

Intended Use

NPM (Phospho-Thr234) Colorimetric Cell-Based ELISA Kit allows for the qualitative detection of NPM (Phospho-Thr234) and the effects that certain stimulation conditions have on NPM (Phospho-Thr234) expression in different cell lines.

Contents of Kit

1. 96-Well Cell Culture Clear-Bottom Microplate: 2 Plates.
2. 10x TBS: 24 mL (10x), Clear.
3. Quenching Buffer, 24 mL (1x), Clear.
4. Blocking Buffer, 50 mL (1x), Clear.
5. 10x Wash Buffer, 50 mL (10x), Clear.
6. 100x Anti-NPM (Phospho-Thr234) Antibody (Rabbit Polyclonal) 60 μL (100x) Red.
7. 100x Anti-NPM Antibody (Rabbit Polyclonal) 60 μL (100x) Purple.
8. 100x Anti-GAPDH Antibody (Mouse Monoclonal) 60 μL (100x) Green.
9. HRP-Conjugated Anti-Rabbit IgG Antibody, 12 mL (1x), Glass.
10. HRP-Conjugated Anti-Mouse IgG Antibody, 12 mL (1x), Glass.
11. Primary Antibody Diluent, 12 mL (1x), Clear.
12. Ready-to-Use Substrate, 12 mL (1x), Brown.
13. Stop Solution, 12 mL (1x), Clear.
14. Crystal Violet Solution, 12 mL (1x), Glass.
15. SDS Solution, 24 mL (1x), Clear.
16. Adhesive Plate Seals, 4 Seals.

Storage

4°C/6 Months

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Significance of FLT3-tyrosine kinase domain mutation as a prognostic factor for acute myeloid leukemia

INTERNATIONAL JOURNAL OF HEMATOLOGY

Authors: Sakaguchi, Masahiro; Yamaguchi, Hiroki; Kuboyama, Marika; Najima, Yuho; Usuki, Kensuke; Ueki, Toshimitsu; Oh, Iekuni; Mori, Shinichiro; Kawata, Eri; Uoshima, Nobuhiko; Kobayashi, Yutaka; Kako, Shinichi; Tajika, Kenji; Shono, Katsuhiro; Kayamori, Kensuke; Hagihara, Masao; Kanda, Junya; Uchiyama, Hitoji; Kuroda, Junya; Uchida, Naoyuki; Kubota, Yasushi; Kimura, Shinya; Kurosawa, Saiko; Date, Kenta; Nakajima, Nana; Marumo, Atsushi; Omori, Ikuko; Fujiwara, Yusuke; Terada, Kazuki; Yui, Shunsuke; Wakita, Satoshi; Arai, Kunihito; Kitano, Tomoaki; Kakihana, Kazuhiko; Kanda, Yoshinobu; Ohashi, Kazuteru; Fukuda, Takahiro; Inokuchi, Koiti

Abstract

The prognostic significance of FLT3-tyrosine kinase domain (TKD) mutations remains unknown. To investigate the prognostic impact of FLT3-TKD, 676 de novo acute myeloid leukemia (AML), we retrospectively analyzed cases and conducted a review of the literature. Of the 676 de novo AML cases, 34 (5.0%) were FLT3-TKD-positive; both FLT3-TKD and FLT3-ITD were noted in only two cases (0.3%). Although no significant differences in relapse-free survival (RFS) were noted, FLT3-TKD-positive cases showed better prognoses than FLT3-ITD-positive cases (FLT3-TKD versus FLT3-ITD, p = 0.152). For overall survival (OS), although FLT3-TKD-positive cases showed prognoses similar to those for FLT3-WT cases, their prognoses were significantly better than those of FLT3-ITD-positive cases (FLT3-TKD versus FLT3-ITD, p = 0.032). Moreover, the 5-year OS for FLT3-TKD-positive cases was 46.1%, indicating that this as an intermediate prognosis group. Although no reports from Asia have indicated a frequency of FLT3-TKD-positive cases > 10%, several reports from Europe and the United States have indicated frequencies > 10%. This suggests the possibility that FLT3-TKD-positive cases are less common in Asia than in Europe and the United States. We anticipate that in the future, the appearance of targeting agents, such as FLT3 inhibitors, will improve the prognosis of FLT3-TKD-positive AML relative to that of FLT3-WT AML.

NPM-ALK Is a Key Regulator of the Oncoprotein FOXM1 in ALK-Positive Anaplastic Large Cell Lymphoma

CANCERS

Authors: Haque, Moinul; Li, Jing; Huang, Yung-Hsing; Almowaled, Meaad; Barger, Carter J.; Karpf, Adam R.; Wang, Peng; Chen, Will; Turner, Suzanne D.; Lai, Raymond

Abstract

Forkhead Box M1 (FOXM1) is an oncogenic transcription factor implicated in the pathogenesis of solid and hematologic cancers. In this study, we examined the significance of FOXM1 in NPM-ALK-positive anaplastic large cell lymphoma (NPM-ALK + ALCL), with a focus on how it interacts with NPM-ALK, which is a key oncogenic driver in these tumors. FOXM1 was expressed in NPM-ALK + ALCL cell lines (5/5), patient samples (21/21), and tumors arising in NPM-ALK transgenic mice (4/4). FOXM1 was localized in the nuclei and confirmed to be transcriptionally active. Inhibition of FOXM1 in two NPM-ALK + ALCL cells using shRNA and pharmalogic agent (thiostrepton) resulted in reductions in cell growth and soft-agar colony formation, which were associated with apoptosis and cell-cycle arrest. FOXM1 is functionally linked to NPM-ALK, as FOXM1 enhanced phosphorylation of the NPM-ALK/STAT3 axis. Conversely, DNA binding and transcriptional activity of FOXM1 was dependent on the expression of NPM-ALK. Further studies showed that this dependency hinges on the binding of FOXM1 to NPM1 that heterodimerizes with NPM-ALK, and the phosphorylation status of NPM-ALK. In conclusion, we identified FOXM1 as an important oncogenic protein in NPM-ALK+ ALCL. Our results exemplified that NPM-ALK exerts oncogenic effects in the nuclei and illustrated a novel role of NPM1 in NPM-ALK pathobiology.