ABN991
Anti-phospho GLUT-1 Antibody (Ser226)
from rabbit, purified by affinity chromatography
Synonym(s):
Solute carrier family 2, facilitated glucose transporter member 1, Glucose transporter type 1, erythrocyte/brain, GLUT-1, HepG2 glucose transporter, Human T-cell leukemia virus I and II receptor, Receptor for HTLV-1 and HTLV-2, phospho GLUT-1 (Ser226)
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All Photos(3)
About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
rabbit
Quality Level
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
purified by
affinity chromatography
species reactivity
mouse, human
species reactivity (predicted by homology)
horse (based on 100% sequence homology), canine (based on 100% sequence homology), bovine (based on 100% sequence homology), Xenopus (based on 100% sequence homology), rat (based on 100% sequence homology), rabbit (based on 100% sequence homology)
technique(s)
immunocytochemistry: suitable
inhibition assay: suitable (peptide)
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
phosphorylation (pSer226 )
Gene Information
human ... SLC2A1(6513)
General description
Solute carrier family 2, facilitated glucose transporter member 1 (UniProt P11166; also known as Glucose transporter type 1 erythrocyte/brain, GLUT-1, HepG2 glucose transporter, Human T-cell leukemia virus I and II receptor, Receptor for HTLV-1 and HTLV-2) is encoded by the SLC2A1 (also known as DYT9, DYT17, DYT18, EIG12, GLUT, GLUT1, HTLVR, GLUT1DS, PED) gene (Gene ID 6513) in human. Glucose transporters (GLUT-1 to GLUT-7) constitute a family of integral membrane glycoproteins that facilitate cellular glucose uptake. In addition to mediating glucose uptake in adult tissues, GLUT-1 is the predominant glucose transporter in embryonic and fetal tissues. Two forms of GLUT-1 are found in human frontal cortex, the 55 kDa form of GLUT-1 regulates import of glucose from blood to brain across the endothelial cells of the blood-brain barrier (BBB), whereas the 45 kDa form of GLUT-1 predominantly regulates nonvascular glial glucose uptake.
Immunogen
Epitope: pSer226 in the fourth cytoplasmic domain (Loop 6).
KLH-conjugated linear peptide corresponding to a fourth cytoplasmic domain (Loop 6) sequence of human GLUT-1 with phosphorylated Ser226.
Application
Peptide Inhibition Analysis: 2.0 µg/mL from a representative lot detected Ser226 phosphorylated GLUT-1 in lysates from PMA-treated HeLa cells. Pre-incubation of the antibody with the immunogen peptide, but not the correspoding non-phosphorylated peptide, blocked the detection of the phospho GLUT-1 band.
Western Blotting Analysis: An 1:200 dilution (5 µg/mL) from a representative lot detected TPA-induced phosphorylation of wild-type GLUT-1, but not GLUT-1 with S226A mution in lysates from Rat2 fibroblasts expsssing the respective constructs via retrovirus-mediated transfection (Courtesy of Dr. Richard C. Wang, UT Southwestern Medical Center, Dallas, TX).
Western Blotting Analysis: An 1:200 dilution (5 µg/mL) from a representative lot detected a time-dependent GLUT-1 Ser226 phosphorylation induction in serum-starved human umbilical vein endothelial cells (HUVECs) and human aortic endothelial cells (HAECs) upon VEGF treatment (Courtesy of Dr. Richard C. Wang, UT Southwestern Medical Center, Dallas, TX).
Western Blotting Analysis: A representative lot detected PKC activation-induced GLUT-1 Ser226 phosphorylation in human aortic endothelial cells (HAECs) upon TPA (Cat. No. 500582 & 524400) treatment only the in the absence, but not in the presence, of PKC inhibitor Go 6983 (Cat. No. 365251) (Lee, E.E., et al. (2015). Mol. Cell. 58(5):845-853).
Western Blotting Analysis: A representative lot detected a time-dependent GLUT-1 Ser226 phosphorylation induction in serum-starved human umbilical vein endothelial cells (HUVECs) upon VEGF or angiotensin II treatment (Lee, E.E., et al. (2015). Mol. Cell. 58(5):845-853).
Western Blotting Analysis: A representative lot detected comparable Ser226 phosphorylation induction of exogenously expressed wild-type GLUT-1 or K526E mutant in transfected Rat2 fibroblasts upon PKC activator TPA (Cat. No. 500582 & 524400) treatment (Cat. No. 365251) (Lee, E.E., et al. (2015). Mol. Cell. 58(5):845-853).
Western Blotting Analysis: A representative lot detected PKC activator TPA-induced GLUT-1 Ser226 phosphorylation in serum-starved HeLa, human primary cardiac endothelial cells, EA.hy926 human endothelial cells, and bEnd.3 mouse brain endothelial cells (Lee, E.E., et al. (2015). Mol. Cell. 58(5):845-853).
Western Blotting Analysis: A representative lot detected PKC-catalyzed Ser226 phosphorylation of GST fusion protein containing wild-type GLUT-1 Loop 6 (4th cytoplasmic domain) seuqnce, but not GST-Loop 6 fusions with R223P, R223Q, R223W, or S226A mutation, in in vitro kinase assays (Lee, E.E., et al. (2015). Mol. Cell. 58(5):845-853).
Western Blotting Analysis: A representative lot detected a time-dependent GLUT-1 Ser226 phosphorylation induction in serum-starved human aortic endothelial cells (HAECs) upon VEGF treatment (Lee, E.E., et al. (2015). Mol. Cell. 58(5):845-853).
Immunocytochemistry Analysis: A representative lot detected PKC activation-induced GLUT-1 Ser226 phosphorylation in the membrane ruffles of human umbilical vein endothelial cells (HUVECs) upon TPA (Cat. No. 500582 & 524400) treatment (Lee, E.E., et al. (2015). Mol. Cell. 58(5):845-853).
Note: Process lysate samples by warming at 50°C for 10 minutes prior to gel loading. Avoid heating samples at a temperature higher than 60°C, which can cause aggregation of the target protein.
Western Blotting Analysis: An 1:200 dilution (5 µg/mL) from a representative lot detected TPA-induced phosphorylation of wild-type GLUT-1, but not GLUT-1 with S226A mution in lysates from Rat2 fibroblasts expsssing the respective constructs via retrovirus-mediated transfection (Courtesy of Dr. Richard C. Wang, UT Southwestern Medical Center, Dallas, TX).
Western Blotting Analysis: An 1:200 dilution (5 µg/mL) from a representative lot detected a time-dependent GLUT-1 Ser226 phosphorylation induction in serum-starved human umbilical vein endothelial cells (HUVECs) and human aortic endothelial cells (HAECs) upon VEGF treatment (Courtesy of Dr. Richard C. Wang, UT Southwestern Medical Center, Dallas, TX).
Western Blotting Analysis: A representative lot detected PKC activation-induced GLUT-1 Ser226 phosphorylation in human aortic endothelial cells (HAECs) upon TPA (Cat. No. 500582 & 524400) treatment only the in the absence, but not in the presence, of PKC inhibitor Go 6983 (Cat. No. 365251) (Lee, E.E., et al. (2015). Mol. Cell. 58(5):845-853).
Western Blotting Analysis: A representative lot detected a time-dependent GLUT-1 Ser226 phosphorylation induction in serum-starved human umbilical vein endothelial cells (HUVECs) upon VEGF or angiotensin II treatment (Lee, E.E., et al. (2015). Mol. Cell. 58(5):845-853).
Western Blotting Analysis: A representative lot detected comparable Ser226 phosphorylation induction of exogenously expressed wild-type GLUT-1 or K526E mutant in transfected Rat2 fibroblasts upon PKC activator TPA (Cat. No. 500582 & 524400) treatment (Cat. No. 365251) (Lee, E.E., et al. (2015). Mol. Cell. 58(5):845-853).
Western Blotting Analysis: A representative lot detected PKC activator TPA-induced GLUT-1 Ser226 phosphorylation in serum-starved HeLa, human primary cardiac endothelial cells, EA.hy926 human endothelial cells, and bEnd.3 mouse brain endothelial cells (Lee, E.E., et al. (2015). Mol. Cell. 58(5):845-853).
Western Blotting Analysis: A representative lot detected PKC-catalyzed Ser226 phosphorylation of GST fusion protein containing wild-type GLUT-1 Loop 6 (4th cytoplasmic domain) seuqnce, but not GST-Loop 6 fusions with R223P, R223Q, R223W, or S226A mutation, in in vitro kinase assays (Lee, E.E., et al. (2015). Mol. Cell. 58(5):845-853).
Western Blotting Analysis: A representative lot detected a time-dependent GLUT-1 Ser226 phosphorylation induction in serum-starved human aortic endothelial cells (HAECs) upon VEGF treatment (Lee, E.E., et al. (2015). Mol. Cell. 58(5):845-853).
Immunocytochemistry Analysis: A representative lot detected PKC activation-induced GLUT-1 Ser226 phosphorylation in the membrane ruffles of human umbilical vein endothelial cells (HUVECs) upon TPA (Cat. No. 500582 & 524400) treatment (Lee, E.E., et al. (2015). Mol. Cell. 58(5):845-853).
Note: Process lysate samples by warming at 50°C for 10 minutes prior to gel loading. Avoid heating samples at a temperature higher than 60°C, which can cause aggregation of the target protein.
This Anti-phospho GLUT-1 Antibody (Ser226) is validated for use in Western Blotting, Peptide Inhibition Assay, Immunocytochemistry for the detection of phospho GLUT-1.
Quality
Evaluated by Western Blotting in HeLa cell lysate.
Western Blotting Analysis: 2.0 µg/mL of this antibody detected Ser226 phosphorylated GLUT-1 in lysates from PMA-treated HeLa cells.
Western Blotting Analysis: 2.0 µg/mL of this antibody detected Ser226 phosphorylated GLUT-1 in lysates from PMA-treated HeLa cells.
Target description
~50 kDa observed. A smeared banding pattern between 45-75 kDa can often be seen, representing target bands with varying degrees of glycosylation.
Other Notes
Concentration: Please refer to lot specific datasheet.
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Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Find documentation for the products that you have recently purchased in the Document Library.
Yunus Saatchi et al.
The American journal of pathology, 193(9), 1195-1207 (2023-06-25)
Although nonrecurrent and recurrent forms of ductal carcinoma in situ (DCIS) of the breast are observed, no evidence-based test can make this distinction. The current retrospective case-control study used archival DCIS samples stained with anti-phospho-Ser226-glucose transporter type 1 and anti-phosphofructokinase
Alexandra M Kraft et al.
American journal of physiology. Cell physiology, 319(5), C910-C921 (2020-09-10)
Some patients treated for ductal carcinoma in situ (DCIS) of the breast will experience cancer recurrences, whereas other patients will not. Unfortunately, current techniques cannot identify which preinvasive lesions will lead to recurrent cancer. Because the mechanism of cancer recurrence
Eunice E Lee et al.
Methods in molecular biology (Clifton, N.J.), 1713, 57-67 (2017-12-09)
Understanding the physiological regulation of glucose transport requires the analysis of transporters, like GLUT1, in diverse tissue types. We document the utility of viral vectors for the stable expression of wild-type and modified GLUT1 transporter in different types of mammalian
De-Dong Li et al.
Cell host & microbe, 30(4), 530-544 (2022-03-23)
Combating fungal pathogens poses metabolic challenges for neutrophils, key innate cells in anti-Candida albicans immunity, yet how host-pathogen interactions cause remodeling of the neutrophil metabolism is unclear. We show that neutrophils mediate renal immunity to disseminated candidiasis by upregulating glucose
Evi Goulielmaki et al.
Nature communications, 11(1), 42-42 (2020-01-04)
DNA damage and metabolic disorders are intimately linked with premature disease onset but the underlying mechanisms remain poorly understood. Here, we show that persistent DNA damage accumulation in tissue-infiltrating macrophages carrying an ERCC1-XPF DNA repair defect (Er1F/-) triggers Golgi dispersal
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