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A\-trans retinoic acid

In 2012, a group of Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, Nebraska, USA examined their growth inhibitory effect of 9-cis retinoic acid (30) and a -trans retinoic acid (29) on the formation and degradation of gap junctions, and on junctional communication in three LNCaP eells of an human androgen-responsive prostate cancer cell line. [Pg.20]

First, the growth inhibitory effect of LNCaP-P cells was around 16-27% for 9-cis retinoic acid (30), around 19-23% for aW-trans retinoic acid (29) and around 17-26% for mibolerone (MB. 48) treatments, respectively, and the growth inhibitory effect of LNCaP-P cells was around 31-38% for 9-cis retinoic acid (30) + mibolerone (MB. 48), around 34-39% for a -trans retinoic acid (29) + mibolerone (MB. 48), and around 35-40% for 9-cis retinoic acid (30) + s -trcms retinoic acid (29) treatments, respectively. [Pg.22]

Stehlin-Gaon, C., D. Wilhnann, D. Zeyer, et al. 2003. A[ -trans Retinoic Acid Is a Ligand for the Orphan Nuclear Receptor Ror(3. Nat Struct Biol 10, no 10 820-25. [Pg.29]

To name retinoids systematically (lUPAC nomenclature), however, a different numbering scheme must be used the carbon atom bonded to the functional group is given number 1. The numbering of carbon atoms by this scheme is shown m structure III for a -trans retinoic acid. Accordingly, the systemic name for a -trans retinoic acid is (al trans) 3,7-dimethyl-9-(2,6,6-trimethylcyclohex-l-en-l-yl)-nona-2,4,6,8-tetraen-l-oic acid, or more simply (all-trans) 3,7-dimethyl-9-(2,6,6-trimethylcyclohexene-l-yl)-2,4,6,8-nonatetraenoic acid. [Pg.5]

Radiolabeled retinoic acid isomers [11,12 H(N)] a -trans retinoic acid is available commercially from Dupont NEN (Stevenage, Hertfordshire, UK) This material can also be used for preparation of the 13-cis and 9-cis isomers [ H] 9-cis retinoic acid is available from Amersham Life Science (Little Chalfont, Buckinghamshire, UK)... [Pg.270]

Smeland EB, Rusten L, Jacobsen SE, Skrede B, Blomhoff R, Wang MY, Funderud S, Kvalheim G, Blomhoff HK (1994) A -trans retinoic acid directly inhibits granulocyte colony-stimulating factor-induced proliferation of CD34+ human hematopoietic progenitor cells. Blood 84 2940-2945... [Pg.140]

Fisher GJ, Reddy AP, Datta SC, Kang S, Yi JY, Chambon P, Voorhees JJ (1995) A -trans retinoic acid and diW-trans retinol induce cellular retinol-binding protein in human skin in vivo. J Invest Dermatol 105 80-86 Kang S, Duell EA, Fisher GJ, Datta SC, Wang ZQ, Reddy AP, Tavakkol A, Yi JY, Griffiths CEM, Elder JT et al (1995) Application of retinol to human skin in vivo induces epidermal hyperplasia and cellular retinoid binding proteins characteristic of retinoic acid but without measurable retinoic acid levels or irritation. J Invest Dermatol 105 549-556... [Pg.157]

Kurlandsky SB, Xiao JH, Duell EA, Voorhees JJ, Fisher GJ (1994) Biological activity of dW-trans retinol requires metabolic conversion to A -trans retinoic acid and is mediated through activation of nuclear retinoid receptors in human keratinocytes. J Biol Chem 269 32821-32827... [Pg.157]

Effects of a -trans retinoic acid and 13-cis retinoic acid on breast cancer cell lines... [Pg.215]

Tallman MS, Andersen J, Schiffer CA, Bloomfield C, Rowe J (1997) A -trans retinoic acid in acute promyelocytic leukemia. New Engl J Med 337 1021-1030... [Pg.240]

Tomas JF, Escudero A, Femandez-Ranada JM (1994) A -trans retinoic acid treatment and Sweett syndrome. Leukemia 8 1596-1597... [Pg.240]

Gander RJ, Gurney JA (1978) A -trans retinoic acid esters and amides. U.S. patent 4,108,880, August 22, 1978. ChemAbstrSS 89892... [Pg.247]

Varani J, Perone P, Griffiths CEM, Inman DR, Fligiel SEG, Voorhees JJ (1994) A -trans retinoic acid stim-... [Pg.276]

Retinoids are needed for cellular differentiation and skin growth. Some retinoids even exert a prophylactic effect on preneoplastic and malignant skin lesions. Fenretlnide (54) is somewhat more selective and less toxic than retinyl acetate (vitamin A acetate) for this purpose. It is synthesized by reaction of all trans-retinoic acid (53), via its acid chloride, with g-aminophe-nol to give ester 54 (13). [Pg.7]

Agents which enhance the host s response against neoplasias or force them to differentiate are termed biological response modifiers. Examples include interleukin 2 which is used to treat renal cell carcinoma, interferon a which is active against hematologic neoplasias, and tretinoin (all-trans retinoic acid) which is a powerful inducer of differentiation in certain leukemia cells by acting on retinoid receptors. Side effects include influenza like symptoms, changes in blood pressure and edema. [Pg.156]

CYP26 consists of three enzymes each representing a separate subfamily (Table 1) probably are all involved in retinoic acid hydroxylation. CYP26A1 is an all trans retinoic acid hydroxylase which degrades retinoic acid, an important signalling molecule for vertebrate development. It acts through retinoic acid receptors. The other CYP26 isozymes are also retinoic acid hydroxylases. [Pg.927]

A most important function of vitamin A is in the control of cell differentiation and mrnover. PsA-trans-retinoic acid and 9-cw-retinoic acid (Figure 45-1) regulate growth, development, and tissue differentiation they have different actions in different tissues. Like the steroid hormones and vitamin D, retinoic acid binds to nuclear receptors that bind to response elements of DNA and regulate the transcription of specific genes. There are two families of nuclear retinoid receptors the retinoic acid receptors (RARs) bind all-rrijw-retinoic acid or 9-c -retinoic acid, and the retinoid X receptors (RXRs) bind 9-cw-retinoic acid. [Pg.483]

Tretinoin, also referred to ATRA, which stands for all-trans-retinoic acid, is a retinoic acid that is not cytotoxic but promotes the maturation of early promyelocytic cells and is specific to the t(15 17) cytogenetic marker. The time to peak concentrations is 1 to 2 hours after an oral dose. The elimination half-life is 21 to 51 minutes.32 These maroon-and-gold capsules are dosed at 45 mg/m2 per day divided into two doses. The most significant side effect is the retinoic acid syndrome, which may occur anywhere from the first couple of days of therapy until the end of therapy and consists of symptoms of... [Pg.1292]

Liu, Y., Chang, R.L., Cui, X.X., Newmark, H.L. and Conney, A.H. 1997. Synergistic effects of curcumin on all-trans retinoic acid- and 1 alpha,25-dihydroxyvitamin D3-induced differentiation in human promyelocytic leukemia HL-60 cells. Oncol Res 9 19-29. [Pg.481]

Baltes S, Nau H, and Lampen A [2004] All-trans retinoic acid enhances differentiation and influences permeability of intestinal Caco-2 cells under serum-free conditions. Dev Growth Differentiation 46 503-514... [Pg.361]

White JA, Ramshaw H, Taimi M, Stangle W, Zhang A, et al. 2000. Identification of the human cytochrome P450, P450RAI-2, which is predominantly expressed in the adult cerebellum and is responsible for all-trans-retinoic acid metabolism. Proc Natl Acad Sci USA 97 6403-6408. [Pg.92]

Tretinoin (Trans-Retinoic Acid Vitamin A Acid)... [Pg.2051]

There are many retinol containing preparations to treat vitamin deficiency states. Retinoids are also used to treat dermatological diseases like acne, psoriasis, Darier s disease, and ichthyosis. Tretinoin, all-trans-retinoic acid, is a topical preparation while isotretinoin or 13-cis-retinoic acid, and etretinate are available for oral administration. [Pg.476]

Fig. 4.6. HRE structure of the RXR heterodimer. Shown is the consensus sequence of the HREs of the RXR heterodimers (see Fig. 4.7) and the different possible arrangements of the hexameric half-site sequences. The hexamers can be arranged palindromically as inverted repeats (a), as everted repeats (b), or as direct repeats (c). n indicates the number of base pairs that lie between the two hexamers. RXR receptor for 9-ds retinoic acid RAR receptor for all-trans retinoic acid T3R receptor for the T3 hormon PPAR peroxisome prohferator-activated receptor VDR receptor for vitamin D3. Fig. 4.6. HRE structure of the RXR heterodimer. Shown is the consensus sequence of the HREs of the RXR heterodimers (see Fig. 4.7) and the different possible arrangements of the hexameric half-site sequences. The hexamers can be arranged palindromically as inverted repeats (a), as everted repeats (b), or as direct repeats (c). n indicates the number of base pairs that lie between the two hexamers. RXR receptor for 9-ds retinoic acid RAR receptor for all-trans retinoic acid T3R receptor for the T3 hormon PPAR peroxisome prohferator-activated receptor VDR receptor for vitamin D3.
The DNA binding element of the nuclear receptors for all-trans retinoic acid, for 9-cis retinoic acid, for the T3 hormone and for the vitamin D3 hormone usually exhibit a direct repeat of the recognition sequence, resulting in formation of heterodimers on the DNA (fig. 4.7b). One of the partners in the heterodimer is always the receptor for 9-cis retinoic acid, RXR, and which usually occupies the 5 side of the HRE. [Pg.157]

The receptors for all-trans retinoic acid, vitamin D3 and the Ts-hormone (as well as other receptors of this class, see table 4.1) usually perform their regulatory function as heterodimers. RXR plays a special role in the formation of heterodimers the receptor for 9-cis retinoic acid is usually one of the binding partners in the heterodimer. [Pg.168]

See other pages where A\-trans retinoic acid is mentioned: [Pg.803]    [Pg.44]    [Pg.245]    [Pg.152]    [Pg.1451]    [Pg.443]    [Pg.803]    [Pg.44]    [Pg.245]    [Pg.152]    [Pg.1451]    [Pg.443]    [Pg.388]    [Pg.425]    [Pg.301]    [Pg.110]    [Pg.196]    [Pg.314]    [Pg.194]    [Pg.475]    [Pg.249]    [Pg.149]    [Pg.151]    [Pg.158]    [Pg.1294]    [Pg.89]    [Pg.175]   


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A-Retinoic acid

Retinoic

Retinoic acid

Trans-retinoic acid

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