ABE1971
Anti-phospho TFEB (Ser142) Antibody
from rabbit, purified by affinity chromatography
Synonym(s):
Transcription factor EB, Ser142 phosphorylated, bHLHe35, Ser142 phosphorylated, Class E basic helix-loop-helix protein 35, Ser142 phosphorylated
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
biological source
rabbit
Quality Level
antibody product type
primary antibodies
clone
polyclonal
purified by
affinity chromatography
species reactivity
human
species reactivity (predicted by homology)
rabbit (based on 100% sequence homology), bovine (based on 100% sequence homology), rat (based on 100% sequence homology), mouse (based on 100% sequence homology), nonhuman primates (based on 100% sequence homology)
technique(s)
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
dry ice
Gene Information
human ... TFEB(7942)
General description
Transcription factor EB (UniProt P19484; also known as bHLHe35, Class E basic helix-loop-helix protein 35) is encoded by the TFEB (also known as ALPHATFEB, BHLHE35, TCFEB) gene (Gene ID 7942) in human. TFEB is a basic Helix-Loop-Helix (bHLH) leucine zipper transcription factor that plays a major role in the regulation of lysosomal biogenesis. TFEB is also a main player in the transcriptional response to starvation and controls autophagy by positively regulating autophagosome formation and autophagosome-lysosome fusion. TFEB is phosphorylated by mTORC1 and ERK at Ser142, which prevents its nuclear translocation. Pharmacological inhibition of mTORC1, as well as starvation and lysosomal disruption, activates TFEB nuclear translocation. Similarly, the serine-threonine kinase RIP1/RIPK1 is shown to suppress basal autophagic flux by activating ERK, which in turn phosphorylates TFEB at Ser142 and thereby prevents TFEB-mediated transcription of gene products involved in autophagy.
Specificity
This polyclonal antibody detected a target band only in lysates from cells expressing wild-type TFEB, but not cells expressing TFEB with S142A mutation (Yonekawa, T., et al. (2015). Nat. Cell Biol. EMBO Rep. 16(6):700-708). The target phosphorylation site is conserved in murine (Ser141; UniProt Q9R210) and rat (Ser142; UniProt F7F5J1) TFEB protein, but not present in human TFEB spliced isoform 2 (UniProt P19484-2).
Immunogen
Epitope: pSer142.
KLH-conjugated linear peptide corresponding to a human TFEB sequence containing the phosphorylated Ser142.
Application
Anti-phospho TFEB (Ser142) Antibody is an antibody against phospho TFEB for use in Western Blotting.
Western Blotting Analysis: A representative lot detected Ser142 phosphorylated TFEB in control HeLa cells, but not in RIP1-deficient HeLa cells following RIP1 shRNAs treatment (Yonekawa, T., et al. (2015). Nat. Cell Biol. EMBO Rep. 16(6):700-708).
Western Blotting Analysis: A representative lot detected Ser142 phosphorylation induction of exogenously expressed wild-type, but not S142A mutant, TFEB (with 3xFLAG tag) upon amino acids addition to nutrient starved HEK293T transfectants (Settembre, C., et al. (2012). EMBO J. 31(5):1095-1108).
Western Blotting Analysis: A representative lot detected nutrient-induced Ser142 phosphorylation of exogenously expressed TFEB (with 3xFLAG tag) in starved HeLa transfectants. Pretreatment of mTOR inhibitor Torin1 (Cat. No. 475991) completely prevented nutrient-induced TFEB Ser142 phosphorylation, a weaker mTOR inhibitor Rapamycin (Cat. No. 553210) partially supperessed the Ser142 phosphorylation induciton (Settembre, C., et al. (2012). EMBO J. 31(5):1095-1108).
Western Blotting Analysis: A representative lot detected Ser142 phosphorylation induction of exogenously expressed wild-type, but not S142A mutant, TFEB (with 3xFLAG tag) upon amino acids addition to nutrient starved HEK293T transfectants (Settembre, C., et al. (2012). EMBO J. 31(5):1095-1108).
Western Blotting Analysis: A representative lot detected nutrient-induced Ser142 phosphorylation of exogenously expressed TFEB (with 3xFLAG tag) in starved HeLa transfectants. Pretreatment of mTOR inhibitor Torin1 (Cat. No. 475991) completely prevented nutrient-induced TFEB Ser142 phosphorylation, a weaker mTOR inhibitor Rapamycin (Cat. No. 553210) partially supperessed the Ser142 phosphorylation induciton (Settembre, C., et al. (2012). EMBO J. 31(5):1095-1108).
Quality
Evaluated by Western Blotting in lysates from TFEB-transfected HEK293 cells.
Western Blotting Analysis: A 1:12500 dilution of this antibody detected Ser142 phosphorylation of FLAG-tagged human TFEB in 10 µg lysate from transfecgted HEK293 cells.
Western Blotting Analysis: A 1:12500 dilution of this antibody detected Ser142 phosphorylation of FLAG-tagged human TFEB in 10 µg lysate from transfecgted HEK293 cells.
Target description
~60 kDa observed (with 3xFLAG tag). 52.87 kDa calculated. Uncharacterized band(s) may appear in some lysates.
Other Notes
Concentration: Please refer to lot specific datasheet.
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Hua Shen et al.
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The development of resistance to EGFR Tyrosine kinase inhibitors (TKIs) in NSCLC with activating EGFR mutations is a critical limitation of this therapy. In addition to genetic alterations such as EGFR secondary mutation causing EGFR-TKI resistance, compensatory activation of signaling
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Recent evidence demonstrates that alcohol activates the mechanistic target of rapamycin (mTOR) and impairs hepatic transcription factor EB (TFEB) reducing autophagy and contributing to alcohol-induced liver injury. Trehalose, a disaccharide, activates TFEB and protects against diet-induced nonalcoholic fatty liver disease
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Bi-allelic GBA1 mutations cause Gaucher's disease (GD), the most common lysosomal storage disorder. Neuronopathic manifestations in GD include neurodegeneration, which can be severe and rapidly progressive. GBA1 mutations are also the most frequent genetic risk factors for Parkinson's disease. Dysfunction
Wencong Song et al.
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Objective- TFEB (transcription factor EB) was recently reported to be induced by atheroprotective laminar flow and play an anti-atherosclerotic role by inhibiting inflammation in endothelial cells (ECs). This study aims to investigate whether TFEB regulates endothelial inflammation in diabetic db/db
Xu-Jia Zeng et al.
Journal of cellular and molecular medicine, 24(12), 7000-7014 (2020-05-13)
Spatial recognition memory impairment is an important complication after traumatic brain injury (TBI). We previously found that spatial recognition memory impairment can be alleviated in adenosine A2A receptor knockout (A2A R KO) mice after TBI, but the mechanism remains unclear.
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