diphtheria/tyrosine

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A diphtheria toxin interleukin-3 fusion protein synergizes with tyrosine kinase inhibitors in killing leukemic progenitors from BCR/ABL positive acute leukemia.

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Ingia / Ingia

Despite initial remissions, most patients with Ph chromosome positive (Ph(+)) acute leukemia (AL) become refractory to tyrosine kinase inhibitors (TKIs) such as imatinib and dasatinib. This study was designed to determine if targeting the interleukin-3 receptor (IL-3R) with a diphtheria toxin fusion

Active-site mutations of diphtheria toxin: role of tyrosine-65 in NAD binding and ADP-ribosylation.

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Ingia / Ingia

Previous studies have suggested that tyrosine-65 (Tyr-65) of diphtheria toxin (DT) is located at the active site. To investigate the role of Tyr-65 in NAD binding and the ADP-ribosylation of elongation factor-2 (EF-2), we changed this residue to alanine and phenylalanine by site-directed mutagenesis

Tyrosine 65 is photolabeled by 8-azidoadenine and 8-azidoadenosine at the NAD binding site of diphtheria toxin.

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Ingia / Ingia

8-Azidoadenine and 8-azidoadenosine, two photoactivatable derivatives of adenine and adenosine, are competitive inhibitors of diphtheria toxin of similar potency with respect to their parent compounds. On irradiation, the two tritium-labeled photoactivatable azidoadenines bind covalently and

[Demonstration of tyrosine in the enzymatic site of diphtheria toxin].

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Ingia / Ingia

DT(270-326) , a Truncated Diphtheria Toxin, Increases Blood-Tumor Barrier Permeability by Upregulating the Expression of Caveolin-1.

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Ingia / Ingia

The nontoxic mutant of diphtheria toxin (DT) has been demonstrated to act as a receptor-specific carrier protein to delivery drug into brain. Recent research showed that the truncated "receptorless" DT was still capable of being internalized into cells. This study investigated the effects and

Suppression of single and double nonsense mutations introduced into the diphtheria toxin A-chain gene: a potential binary system for toxin gene therapy.

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Ingia / Ingia

We have previously shown that ablation of specific cells can be achieved through the transcriptionally regulated expression of the diphtheria toxin A-chain (DT-A) gene in both cell culture and transgenic mice. Such targeted toxin gene expression provides a novel approach to cancer and acquired

Rat hepatoma cell variants resistant to insulin-diphtheria toxin A fragment conjugates. Genetic evidence for the separate pathways for insulin receptor-mediated mitogenic and hormonal stimulation.

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Ingia / Ingia

The rat hepatoma H35 cells in serum-free medium produce tyrosine aminotransferase (TAT) and initiate DNA synthesis and cell division upon exposure to 10(-9)-10(-10) M insulin. This insulin-dependent hormonal and mitogenic stimulation is through the insulin receptors and not through the receptors for

Reversion of recombinant toxoids: mutations in diphtheria toxin that partially compensate for active-site deletions.

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Ingia / Ingia

Deleting an important active-site residue of diphtheria toxin, glutamic acid-148, reduces the toxin's ADP-ribosyltransferase activity by a factor of greater than 10(4). We considered using this mutation to construct a recombinant toxoid for expression by live attenuated vaccines and explored

Investigations into the relationship between structure and function of diphtheria toxin.

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Ingia / Ingia

Studies on the structure-function relationship of diphtheria toxin are reported. New methods are described for the preparation of pure intact ("unnicked") toxin and for the preparation of the individual A and B chains. A biological assay method for the B chain is also presented, as well as a method

Stimulation of proliferation of a human osteosarcoma cell line by exogenous acidic fibroblast growth factor requires both activation of receptor tyrosine kinase and growth factor internalization.

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Ingia / Ingia

U2OS Dr1 cells, originating from a human osteosarcoma, are resistant to the intracellular action of diphtheria toxin but contain toxin receptors on their surfaces. These cells do not have detectable amounts of fibroblast growth factor receptors. When these cells were transfected with fibroblast

Targeting c-kit receptor in neuroblastomas and colorectal cancers using stem cell factor (SCF)-based recombinant bacterial toxins.

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Ingia / Ingia

Autocrine activation of c-kit (KIT receptor tyrosine kinase) has been postulated to be a potent oncogenic driver in small cell lung cancer, neuroblastoma (NB), and poorly differentiated colorectal carcinoma (CRC). Although targeted therapy involving tyrosine kinase inhibitors (TKIs) such as imatinib

A preliminary evaluation of alternative adjuvants to alum using a range of established and new generation vaccine antigens.

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Ingia / Ingia

Although alum is the most commonly used vaccine adjuvant, it has some limitations for use with the next generation recombinant antigens. We explored the use of alternative adjuvant formulations (poly lactide co-glycolide (PLG) microparticles, MF59 emulsion, CAP and l-tyrosine suspension) in

[Activation of the cell proliferation program by acidic fibroblast growth factor (aFGF)].

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Ingia / Ingia

Acidic fibroblast growth factor belongs to the fibroblast growth factor family. It is a potent mitogenic agent. The growth factor acts through activation of specific cell-surface receptors leading to intracellular tyrosine phosphorylation cascade. In addition to its extracellular action, however,

Update in childhood acute myeloid leukemia: recent developments in the molecular basis of disease and novel therapies.

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Ingia / Ingia

Childhood acute myeloid leukemia is a heterogeneous group of disorders that remains challenging to treat. There are multiple common genetic alterations in childhood acute myeloid leukemia. These include chromosomal translocations affecting RUNX1-CBFbeta, RARalpha, and MLL. There are known activating

Effect of ghrelin on the motor deficit caused by the ablation of nigrostriatal dopaminergic cells or the inhibition of striatal dopamine receptors.

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Ingia / Ingia

Ghrelin plays roles in a wide range of central functions by activating the growth hormone secretagogue receptor (GHSR). This receptor has recently been found in the substantia nigra (SN) to control dopamine (DA)-related physiological functions. The dysregulation of DA neurons in the SN pars compacta

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