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Promyelocytic leukemia protein

Louria-Hayon, L, et al.. The Promyelocytic Leukemia Protein Protects p53 from Mdm2-mediated Inhibition and Degradation. J Biol Chem, 2003, 278(35), 33134-41. [Pg.90]

Transcription regulators are also known to be sumoylated. One of tbe early studies of tbis phenomenon showed that promyelocytic leukemia protein (PML) is a substrate for SUMO conjugation. Once SUMO is attached to the PML protein it is directed to a subdomain of tbe nucleus called tbe PML oncogenic domain (POD). It is thought that POD localization of the PML protein allows it to recruit other proteins such as transcription factors. Transcription factors in the POD can activate or inhibit transcription. Another transcription factor known to be sumoylated is Sp3. ° SUMO also has roles in chromatin condensation and interphase chromosome organization. ... [Pg.731]

He P, Liu Y, Zhang M, Wang X, Xi J, Wu D, Li J, Cao Y. Interferon-gamma enhances promyelocytic leukemia protein expression in acute promyelocytic cells and cooperates with allotrans-retinoic acid to induce maturation of NB4 and NB4-R1 cells. Exp Ther Med. 2012 3 776-80. [Pg.710]

Grant S, Turner A, Bartimole TM, Nelms P, Joe VC, Jarvis WD (1994) Modulation of l-p-D-arabinofiiranosylcytosine-induced apoptosis in human promyelocytic leukemia cells by staurosporine and other inhibitors of protein kinase C. Oncol Res 6 87-99... [Pg.72]

Jarvis, W.D., Turner, A.J., Povirk, L.F., Traylor, R.S., and Grant, S., Induction of apoptotic DNA fragmentation and cell death in HL-60 human promyelocytic leukemia cells by pharmacological inhibitors of protein kinase C, Cancer Res., 54, 1707, 1994. [Pg.178]

Chen GQ, Zhu J, Shi XG et al (1996) In vitro studies on cellular and molecular mechanisms of arsenic trioxide (As203) in the treatment of acute promyelocytic leukemia As203 induces NB4 cell apoptosis with downregulation of Bcl-2 expression and modulation of PML-RARa/PML proteins. Blood 88 1052-1061... [Pg.20]

As an alternative to using synthetic analogs for disease treatment, the natural ligand for the retinoic acid receptor, all-irans-retinoic acid (ATRA), is used effectively in the treatment of acute promyelocytic leukemia (APL) (73). Chromosomal translocations in APL patients are responsible for the cellular transformation in this disease. The transformation results in a fusion of the retinoic acid receptor alpha (RARa) with another protein (73). Treatment of APL patients with pharmacologic doses of ATRA induces complete remission by restoring normal granulocytic differentiation (74, 75). [Pg.1856]

The second cannabinoid receptor sub-type, CB2, was derived from a human promyelocytic leukemia cell HL60 cDNA library (Munro et al. 1993). The human CB2 receptor exhibits 68% identity to the human CBi receptor within the transmembrane regions, 44% identity throughout the whole protein. The CB2 receptor in both rat (Griffin et al. 2000) and mouse (Shire et al. 1996) has been cloned as well. A helix net representation of the human CB2 receptor sequence is presented in Fig. 2. Unlike the CB 1 receptor, which is highly conserved across human, rat, and... [Pg.248]

ATRA (1) (Tretinoin) acne, photodamage, acute promyelocytic leukemia (AML) RAR agonist, protein synthesis antagonist, microbial collagenase inhibitor launched AP Pharma, Johnson Johnson, HofF-mann-La Roche, Myland Labs... [Pg.393]

Arsenic trioxide is an antineoplastic agent that causes morphological changes and DNA fragmentation characteristic of apoptosis in NB4 human promyelocytic leukemia cells in vitro. Arsenic trioxide also causes damage or degradation of the fusion protein PML/RAR alpha. It is indicated in the treatment of refractory or relapsed acute promyelocytic leukemia (APT). [Pg.89]


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See also in sourсe #XX -- [ Pg.248 ]




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