INABILITY OF INSULIN AND INSULIN-LIKE GROWTH FACTOR-I TO STIMULATE SUGAR OR AMINO-ACID-TRANSPORT AND THYMIDINE INCORPORATION IN CULTURED MYELOMA CELLS

被引:1
|
作者
LECKETT, B [1 ]
GERMINARIO, RJ [1 ]
机构
[1] SIR MORTIMER B DAVIS JEWISH HOSP,LADY DAVIS INST MED RES,3755 COTE ST CATHERINE RD,MONTREAL H3T 1E2,QUEBEC,CANADA
关键词
CULTURED MYELOMA CELLS; INSULIN AND IGF-1 BINDING AND ACTION; SUGAR TRANSPORT; AMINO ACID TRANSPORT; DNA SYNTHESIS;
D O I
10.1139/o91-127
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
NS-1 mouse plasmacytoma cells were examined for their insulin and insulinlike growth factor-1 (IGF-1) binding characteristics and ability to produce peptide-dependent cellular effects. At concentrations of labelled insulin (i.e., 1.7 x 10(-10) M) or IGF-1 (i.e., 1.5 x 10(-10) M), NS-1 cells specifically bind 0.2 +/- 0.06 fmol insulin per 10(6) cells (n = 7), where little, if any, IGF-1 specific binding was observed (0.02 +/- 0.01 fmol/10(6) cells) (n = 3). Additionally, the data indicate that the total number of insulin binding sites per cell was 3200 +/- 390 (n = 3). Insulin was employed at various concentrations (6.7-667 nM) and failed to stimulate either sugar or amino acid transport. Insulin at low concentrations (i.e., 6.7 or 67 nM) did not stimulate DNA synthesis, yet a small but significant increase was observed at a concentration of 667 nM insulin. IGF-1 did not stimulate DNA synthesis at all concentrations employed (1.4-143 nM). In summary, there exists a small but significant number of insulin receptors, little insulin-stimulated DNA synthesis, and no apparent insulin stimulation of sugar or amino acid transport. Also, since there is no significant IGF-1 binding and no IGF-1 stimulation of DNA synthesis, these findings indicate that this cell line might be a good candidate for the study of insulin receptor function as a transfection recipient of insulin receptor genes.
引用
收藏
页码:859 / 863
页数:5
相关论文
共 50 条
  • [21] INSULIN-LIKE GROWTH FACTOR-I AND FACTOR-II STIMULATE GROWTH OF HYPOPHYSECTOMIZED RATS
    SCHOENLE, E
    ZAPF, J
    FROESCH, ER
    DIABETOLOGIA, 1982, 23 (02) : 199 - 199
  • [22] Insulin-like growth factor-I deficiency
    Camacho-Hübner, C
    Savage, M
    HORMONE RESEARCH, 2001, 55 : 17 - 20
  • [23] INSULIN-LIKE GROWTH FACTOR-I IN THE DOG
    EIGENMANN, JE
    FRONTIERS OF HORMONE RESEARCH, 1987, 17 : 161 - 172
  • [24] INSULIN-LIKE GROWTH FACTOR-I AND ERYTHROPOIESIS
    ARON, DC
    BIOFACTORS, 1992, 3 (04) : 211 - 216
  • [25] PURIFICATION OF INSULIN-LIKE GROWTH FACTOR-I
    MORRELL, DJ
    HOLDER, AT
    TAYLOR, AM
    HILL, D
    PULLEN, L
    PREECE, MA
    REGULATORY PEPTIDES, 1984, 9 (04) : 340 - 340
  • [26] Insulin-like growth factor-I resistance
    Jain, S
    Golde, DW
    Bailey, R
    Geffner, ME
    ENDOCRINE REVIEWS, 1998, 19 (05) : 625 - 646
  • [27] Insulin-like growth factor I and insulin stimulate glucose and phosphate transport in rat osteoblastic cells.
    Veldman, CM
    Schmid, C
    JOURNAL OF BONE AND MINERAL RESEARCH, 1996, 11 : T304 - T304
  • [28] Effects of glucose, insulin, and insulin-like growth factor-I on glucose transport activity in cultured rat vascular smooth muscle cells
    Fujiwara, R
    Nakai, T
    ATHEROSCLEROSIS, 1996, 127 (01) : 49 - 57
  • [29] INSULIN-LIKE GROWTH FACTOR-I AND HUMAN LUNG FIBROBLAST-DERIVED INSULIN-LIKE GROWTH FACTOR-I STIMULATE THE PROLIFERATION OF HUMAN LUNG-CARCINOMA CELLS IN-VITRO
    ANKRAPP, DP
    BEVAN, DR
    CANCER RESEARCH, 1993, 53 (14) : 3399 - 3404
  • [30] Insulin-like Growth Factor-I in Growth and Metabolism
    Backeljauw, P.
    Bang, P.
    Dunger, D. B.
    Juul, A.
    Le Bouc, Y.
    Rosenfeld, R.
    JOURNAL OF PEDIATRIC ENDOCRINOLOGY & METABOLISM, 2010, 23 (1-2): : 3 - 16