inactive control peptide tg3 Search Results


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LifeTein Inc inactive control peptide tg3
Peptidomimetic blockade of MYB triggers cell death in T‐ALL. (A, B) Line chart of the ratio of luminescence detected using CellTiter‐Glo cell viability assay (hereafter called relative viability) upon treatment of cell lines with 10–40 µM of MYBMIM (colored line) or its inactive version, named <t>TG3</t> (black line), normalized to the untreated condition. (A) MyPL1 and MyPL2 are murine R26‐Myb tg/tg ; Pten fl/fl ; Lck‐Cre tg/+ T‐ALL cell lines. (B) RPMI‐8402, P12‐Ichikawa, Loucy, KOPT‐K1, and Jurkat are human T‐ALL cell lines. (C) Bar chart showing the relative viability of Jurkat and KOPT‐K1 cells at the beginning of the experiment (0 h), and 48 h later, when treated with either 30 µM (for Jurkat) or 20 µM (for KOPT‐K1) of MYBMIM, TG3, or untreated (CTR 48 h). (D) Stacked bar charts showing the percentage of cells per phase of the cell cycle and (E) the percentage of viable, early apoptotic, or late apoptotic cells at 48 h. A representative result from two independent experiments is shown. (F) Scheme of generation of T‐ALL patient‐derived xenografts (PDXs) through intravenous injections, followed by their ex vivo treatment with either TG3 or MYBMIM. (G) Line chart of the relative viability of T‐ALL PDX with either chromosomal translocation ( TRB::MYB ), genomic gain of MYB ( MYB CNG), or wild‐type MYB ( MYB WT), upon treatment with 10–40 µM of MYBMIM (colored line) or TG3 (black line), normalized to the untreated condition.
Inactive Control Peptide Tg3, supplied by LifeTein Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/inactive+control+peptide+tg3/pmc10924755-74-22-30?v=LifeTein+Inc
Average 90 stars, based on 1 article reviews
inactive control peptide tg3 - by Bioz Stars, 2026-07
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Peptidomimetic blockade of MYB triggers cell death in T‐ALL. (A, B) Line chart of the ratio of luminescence detected using CellTiter‐Glo cell viability assay (hereafter called relative viability) upon treatment of cell lines with 10–40 µM of MYBMIM (colored line) or its inactive version, named TG3 (black line), normalized to the untreated condition. (A) MyPL1 and MyPL2 are murine R26‐Myb tg/tg ; Pten fl/fl ; Lck‐Cre tg/+ T‐ALL cell lines. (B) RPMI‐8402, P12‐Ichikawa, Loucy, KOPT‐K1, and Jurkat are human T‐ALL cell lines. (C) Bar chart showing the relative viability of Jurkat and KOPT‐K1 cells at the beginning of the experiment (0 h), and 48 h later, when treated with either 30 µM (for Jurkat) or 20 µM (for KOPT‐K1) of MYBMIM, TG3, or untreated (CTR 48 h). (D) Stacked bar charts showing the percentage of cells per phase of the cell cycle and (E) the percentage of viable, early apoptotic, or late apoptotic cells at 48 h. A representative result from two independent experiments is shown. (F) Scheme of generation of T‐ALL patient‐derived xenografts (PDXs) through intravenous injections, followed by their ex vivo treatment with either TG3 or MYBMIM. (G) Line chart of the relative viability of T‐ALL PDX with either chromosomal translocation ( TRB::MYB ), genomic gain of MYB ( MYB CNG), or wild‐type MYB ( MYB WT), upon treatment with 10–40 µM of MYBMIM (colored line) or TG3 (black line), normalized to the untreated condition.

Journal: HemaSphere

Article Title: Myb overexpression synergizes with the loss of Pten and is a dependency factor and therapeutic target in T‐cell lymphoblastic leukemia

doi: 10.1002/hem3.51

Figure Lengend Snippet: Peptidomimetic blockade of MYB triggers cell death in T‐ALL. (A, B) Line chart of the ratio of luminescence detected using CellTiter‐Glo cell viability assay (hereafter called relative viability) upon treatment of cell lines with 10–40 µM of MYBMIM (colored line) or its inactive version, named TG3 (black line), normalized to the untreated condition. (A) MyPL1 and MyPL2 are murine R26‐Myb tg/tg ; Pten fl/fl ; Lck‐Cre tg/+ T‐ALL cell lines. (B) RPMI‐8402, P12‐Ichikawa, Loucy, KOPT‐K1, and Jurkat are human T‐ALL cell lines. (C) Bar chart showing the relative viability of Jurkat and KOPT‐K1 cells at the beginning of the experiment (0 h), and 48 h later, when treated with either 30 µM (for Jurkat) or 20 µM (for KOPT‐K1) of MYBMIM, TG3, or untreated (CTR 48 h). (D) Stacked bar charts showing the percentage of cells per phase of the cell cycle and (E) the percentage of viable, early apoptotic, or late apoptotic cells at 48 h. A representative result from two independent experiments is shown. (F) Scheme of generation of T‐ALL patient‐derived xenografts (PDXs) through intravenous injections, followed by their ex vivo treatment with either TG3 or MYBMIM. (G) Line chart of the relative viability of T‐ALL PDX with either chromosomal translocation ( TRB::MYB ), genomic gain of MYB ( MYB CNG), or wild‐type MYB ( MYB WT), upon treatment with 10–40 µM of MYBMIM (colored line) or TG3 (black line), normalized to the untreated condition.

Article Snippet: Murine and human T‐ALL cells were cultured at a density of 10,000 cells/mL and treated with either the peptidomimetic MYBMIM or the inactive control peptide TG3, which were synthetized by LifeTein.

Techniques: Viability Assay, Derivative Assay, Ex Vivo, Translocation Assay