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ABE1400

Sigma-Aldrich

Anti-TFE3

from rabbit, purified by affinity chromatography

别名:

Transcription factor E3, bHLHe33, Class E basic helix-loop-helix protein 33

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About This Item

UNSPSC代码:
12352203
eCl@ss:
32160702

生物来源

rabbit

质量水平

抗体形式

affinity isolated antibody

抗体产品类型

primary antibodies

克隆

polyclonal

纯化方式

affinity chromatography

种属反应性

mouse, human

技术

immunocytochemistry: suitable
western blot: suitable

NCBI登记号

UniProt登记号

运输

ambient

靶向翻译后修饰

unmodified

基因信息

human ... TFE3(7030)

一般描述

Transcription factor E3 (UniProt P19532; also known as bHLHe33, Class E basic helix-loop-helix protein 33, TFE3) is encoded by the TFE3 (also known as BHLHE33) gene (Gene ID 7030) in human. TFE3 contains adjacent helix-loop-helix (HLH) and leucine zipper (LZ) domains flanked by an upstream basic region. It specifically recognizes and binds E-box sequences (5′-CANNTG-3′). TFE3 is ubiquitously expressed and can directly associate with DNA as either homodimers or heterodimers formed with two related proteins, TFEB or TFEC. In association with TFEB, TFE3 activates the expression of CD40L in T-cells, thereby playing a role in T-cell-dependent antibody responses in activated CD4+ T-cells and in thymus-dependent humoral immunity. TFE3 binds to and activates the microE3 motif of the immunoglobulin heavy-chain enhancer to induce B-cell-specific gene transcription and DNA recombination. TFEB is expressed at low levels in the embryo, but is expressed at high levels in the trophoblast cells of the placenta, where it plays a critical role in regulating normal vascularization. It has been shown that the exit from pluripotency is gated by intracellular redistribution of TFE3. Chromosomal aberrations involving TFE3 have been reported in patients with papillary renal cell carcinoma. Ref.: Betschinger, J., et al. (2013). Cell 153, 335-347.

特异性

This polyclonal antibody targets the human TFE3 leucine zipper region sequence.

免疫原

KLH-conjugated linear peptide corresponding to a leucine zipper region sequence of human TFE3.

应用

Anti-TFE3, Cat. No. ABE1400, is a highly specific rabbit polyclonal antibody that targets transcription factor E3 (TFE3) and has been tested in Immunocytochemistry and Western Blotting.
Immunocytochemistry Analysis: A 1:500 dilution from a representative lot detected TFE3 in 4% paraformaldehyde-fixed, 0.5% Triton X-100-permeablized MEF-1 mouse embryonic fibrolasts.
Research Category
Epigenetics & Nuclear Function

质量

Evaluated by Western Blotting in NIH/3T3 nuclear extract.

Western Blotting Analysis: 0.1 µg/mL of this antibody detected TFE3 in 10 µg of NIH/3T3 nuclear extract.

目标描述

~75 kDa observed. Target band size appears larger than the calculated molecular weight of 61.52 kDa due to posttranslational modification. Uncharacterized bands may be observed in some lysate(s).

外形

Affinity purified.
Purified rabbit polyclonal antibody in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

储存及稳定性

Stable for 1 year at 2-8°C from date of receipt.

其他说明

Concentration: Please refer to lot specific datasheet.

免责声明

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Kaushal Asrani et al.
The Journal of clinical investigation, 129(12), 5584-5599 (2019-09-19)
The microphthalmia family of transcription factors (MiT/TFEs) controls lysosomal biogenesis and is negatively regulated by the nutrient sensor mTORC1. However, the mechanisms by which cells with constitutive mTORC1 signaling maintain lysosomal catabolism remain to be elucidated. Using the murine epidermis
Kaiyuan Wu et al.
Autophagy, 17(11), 3707-3724 (2021-02-26)
The mechanisms orchestrating recycling of lysosomes through autophagic lysosome reformation (ALR) is incompletely understood. Previous data show that genetic depletion of BLOC1S1/GCN5L1/BORCS1 increases autolysosome (AL) accumulation. We postulated that this phenotype may manifest due to perturbed ALR. We explored this

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