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Merck

SAB1403709

Sigma-Aldrich

Monoclonal Anti-NKX2-5, (N-terminal) antibody produced in mouse

clone 3A7, purified immunoglobulin, buffered aqueous solution

别名:

CHNG5, CSX, CSX1, NKX2.5, NKX2E, NKX4-1

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About This Item

分類程式碼代碼:
12352203
NACRES:
NA.41

生物源

mouse

共軛

unconjugated

抗體表格

purified immunoglobulin

抗體產品種類

primary antibodies

無性繁殖

3A7, monoclonal

形狀

buffered aqueous solution

分子量

antigen ~40.41 kDa

物種活性

human

技術

indirect ELISA: suitable
western blot: 1-5 μg/mL

同型

IgG2bκ

NCBI登錄號

UniProt登錄號

運輸包裝

dry ice

儲存溫度

−20°C

目標翻譯後修改

unmodified

基因資訊

human ... NKX2-5(1482)

一般說明

Homeobox-containing genes play critical roles in regulating tissue-specific gene expression essential for tissue differentiation, as well as determining the temporal and spatial patterns of development (Shiojima et al., 1995 [PubMed 7665173]). It has been demonstrated that a Drosophila homeobox-containing gene called ′tinman′ is expressed in the developing dorsal vessel and in the equivalent of the vertebrate heart. Mutations in tinman result in loss of heart formation in the embryo, suggesting that tinman is essential for Drosophila heart formation. Furthermore, abundant expression of Csx, the presumptive mouse homolog of tinman, is observed only in the heart from the time of cardiac differentiation. CSX, the human homolog of murine Csx, has a homeodomain sequence identical to that of Csx and is expressed only in the heart, again suggesting that CSX plays an important role in human heart formation.[supplied by OMIM

免疫原

NKX2-5 (NP_004378, 1 a.a. ~ 130 a.a) full length recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.

Sequence
MFPSPALTPTPFSVKDILNLEQQQRSLAAAGELSARLEATLAPSSCMLAAFKPEAYAGPEAAAPGLPELRAELGRAPSPAKCASAFPAAPAFYPRAYSDPDPAKDPRAEKKELCALQKAVELEKTEADNA*

外觀

Solution in phosphate buffered saline, pH 7.4

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儲存類別代碼

10 - Combustible liquids

水污染物質分類(WGK)

WGK 1

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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Zhoufeng Wang et al.
Nature communications, 12(1), 6500-6500 (2021-11-13)
Lung adenocarcinomas (LUAD) arise from precancerous lesions such as atypical adenomatous hyperplasia, which progress into adenocarcinoma in situ and minimally invasive adenocarcinoma, then finally into invasive adenocarcinoma. The cellular heterogeneity and molecular events underlying this stepwise progression remain unclear. In

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