Publications
366 results found
SUTRAVE P, LANA DP, LEFEROVICH J, et al., 1994, SKI AND FIBER-TYPE HYPERTROPHY, Publisher: WILEY-LISS, Pages: 471-471, ISSN: 0730-2312
HOUGHTON LA, ROSENTHAL N, 1994, A HOX SITE WITHIN THE MYOSIN LIGHT-CHAIN 1/3 ENHANCER BINDS DIFFERENT PROTEINS OF MUSCLES DERIVED FROM DISTINCT SOMITIC LINEAGES IN THE MOUSE, Publisher: WILEY-LISS, Pages: 477-477, ISSN: 0730-2312
MCGREW MJ, ROSENTHAL N, 1993, QUANTITATION OF GENOMIC METHYLATION USING LIGATION-MEDIATED PCR, BIOTECHNIQUES, Vol: 15, Pages: 722-&, ISSN: 0736-6205
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- Citations: 12
ROSEN KM, WENTWORTH BM, ROSENTHAL N, et al., 1993, SPECIFIC, TEMPORALLY REGULATED EXPRESSION OF THE INSULIN-LIKE GROWTH FACTOR-II GENE DURING MUSCLE-CELL DIFFERENTIATION, ENDOCRINOLOGY, Vol: 133, Pages: 474-481, ISSN: 0013-7227
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- Citations: 77
ENGERT JC, SERVAES S, ROSENTHAL N, 1993, INDUCTION OF MUSCLE FIBER-SPECIFIC REGULATORY ELEMENTS BY THE SKI ONCOGENE, Publisher: WILEY-LISS, Pages: 219-219, ISSN: 0730-2312
MCGREW M, GRIESHAMMER U, ROSENTHAL N, 1993, DIFFERENTIAL METHYLATION OF THE MYOSIN 1/3 LOCUS IN ADULT SKELETAL-MUSCLES AND DURING MOUSE DEVELOPMENT, Publisher: WILEY-LISS, Pages: 222-222, ISSN: 0730-2312
XIAO YH, GRIESHAMMER U, ROSENTHAL N, 1993, EFFECT OF RETINOIC ACID ON MYOGENESIS DURING MOUSE EMBRYONIC-DEVELOPMENT, Publisher: WILEY-LISS, Pages: 226-226, ISSN: 0730-2312
GONG XH, GRIESHAMMER U, ROSENTHAL N, 1993, A NOVEL MEMBER OF THE BRAHMA FAMILY ENCODES AN E-BOX-SPECIFIC DNA-BINDING PROTEIN, Publisher: WILEY-LISS, Pages: 220-220, ISSN: 0730-2312
BENECKE H, FLIER JS, ROSENTHAL N, et al., 1993, MUSCLE-SPECIFIC EXPRESSION OF HUMAN INSULIN-RECEPTOR IN TRANSGENIC MICE, DIABETES, Vol: 42, Pages: 206-212, ISSN: 0012-1797
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- Citations: 17
SASSOON D, ROSENTHAL N, 1993, DETECTION OF MESSENGER-RNA BY IN-SITU HYBRIDIZATION, GUIDE TO TECHNIQUES IN MOUSE DEVELOPMENT, Vol: 225, Pages: 384-404, ISSN: 0076-6879
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- Citations: 120
KITSIS RN, BUTTRICK PM, ROSENTHAL N, et al., 1992, MYOD CAN TRANSACTIVATE A TARGET GENE IN ADULT-RAT HEART INVIVO, Publisher: AMER HEART ASSOC, Pages: 346-346, ISSN: 0009-7322
GRIESHAMMER U, SASSOON D, ROSENTHAL N, 1992, A TRANSGENE TARGET FOR POSITIONAL REGULATORS MARKS EARLY ROSTROCAUDAL SPECIFICATION OF MYOGENIC LINEAGES, CELL, Vol: 69, Pages: 79-93, ISSN: 0092-8674
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- Citations: 81
DONOGHUE MJ, MERLIE JP, ROSENTHAL N, et al., 1991, ROSTROCAUDAL GRADIENT OF TRANSGENE EXPRESSION IN ADULT SKELETAL-MUSCLE, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 88, Pages: 5847-5851, ISSN: 0027-8424
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- Citations: 77
ERNST H, WALSH K, HARRISON CA, et al., 1991, THE MYOSIN LIGHT CHAIN ENHANCER AND THE SKELETAL ACTIN PROMOTER SHARE A BINDING-SITE FOR FACTORS INVOLVED IN MUSCLE-SPECIFIC GENE-EXPRESSION, MOLECULAR AND CELLULAR BIOLOGY, Vol: 11, Pages: 3735-3744, ISSN: 0270-7306
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- Citations: 42
WENTWORTH BM, DONOGHUE M, ENGERT JC, et al., 1991, PAIRED MYOD-BINDING SITES REGULATE MYOSIN LIGHT CHAIN GENE-EXPRESSION, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 88, Pages: 1242-1246, ISSN: 0027-8424
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- Citations: 194
Boyarsky G, Rosenthal N, Barrett E, et al., 1991, Effect of diabetes on Na(+)-H+ exchange by single isolated hepatocytes., Am J Physiol, Vol: 260, Pages: C167-C175, ISSN: 0002-9513
We used the fluorescent dye 2',7'-bis-(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF) to examine intracellular pH (pHi) regulation in single hepatocytes isolated from control rats and rats with either spontaneous or drug-induced diabetes mellitus (DM). In the absence of CO2-HCO3-, both control and DM cells recovered from cellular acid loads applied by the NH4+ prepulse technique. Because the pHi recovery was blocked by either Na+ withdrawal or ethylisopropylamiloride in both control and DM cells, it was presumably mediated by Na(+)-H+ exchange. In the control cells, the pHi threshold above which the rate of change of pHi (dpHi/dt) was zero was 7.06, and the slope of the dpHi/dt-pHi relationship was -0.030 s-1. In the DM cells, the pHi threshold was 7.22 and the slope was -0.017 s-1. Thus, at pHi values below approximately 6.9, the pHi recovery was slower in the DM cells. Inasmuch as we observed no difference in the cellular buffering power between control and DM cells, diabetes inhibits Na(+)-H+ exchange within this low pHi range. At pHi values above approximately 6.9, however, Na(+)-H+ exchange was apparently stimulated by diabetes. Thus diabetes induces two distinct alterations of Na(+)-H+ exchange, an alkaline shift in pHi threshold and decrease in slope. Treatment of diabetic rats with insulin for 48 h restored both Na(+)-H+ exchange parameters to normal. On the other hand, insulin added in vitro to DM cells for 2-5 h shifted the threshold toward the control value without affecting the slope, thus leading to a further inhibition of Na(+)-H+ exchange over the entire pHi range.(ABSTRACT TRUNCATED AT 250 WORDS)
ROSENTHAL N, BERGLUND EB, WENTWORTH BM, et al., 1990, A HIGHLY CONSERVED ENHANCER DOWNSTREAM OF THE HUMAN MLC1/3 LOCUS IS A TARGET FOR MULTIPLE MYOGENIC DETERMINATION FACTORS, NUCLEIC ACIDS RESEARCH, Vol: 18, Pages: 6239-6246, ISSN: 0305-1048
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- Citations: 90
BRAUN T, BOBER E, WINTER B, et al., 1990, MYF-6, A NEW MEMBER OF THE HUMAN GENE FAMILY OF MYOGENIC DETERMINATION FACTORS - EVIDENCE FOR A GENE-CLUSTER ON CHROMOSOME-12, EMBO JOURNAL, Vol: 9, Pages: 821-831, ISSN: 0261-4189
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- Citations: 435
Rosenthal N, 1989, Muscle cell differentiation, CURRENT OPINION IN CELL BIOLOGY, Vol: 1, Pages: 1094-1101, ISSN: 0955-0674
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- Citations: 43
ROSENTHAL N, KORNHAUSER JM, DONOGHUE M, et al., 1989, MYOSIN LIGHT CHAIN ENHANCER ACTIVATES MUSCLE-SPECIFIC, DEVELOPMENTALLY REGULATED GENE-EXPRESSION IN TRANSGENIC MICE, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 86, Pages: 7780-7784, ISSN: 0027-8424
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- Citations: 120
ROSEN KM, WENTWORTH BM, LAMPERTI ED, et al., 1989, EXPRESSION OF THE IGF-II GENE IN BRAIN AND MUSCLE, SYMP ON MOLECULAR AND CELLULAR BIOLOGY OF INSULIN-LIKE GROWTH FACTORS AND THEIR RECEPTORS, Publisher: PLENUM PRESS DIV PLENUM PUBLISHING CORP, Pages: 219-229
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- Citations: 1
DONOGHUE M, ERNST H, WENTWORTH B, et al., 1988, A MUSCLE-SPECIFIC ENHANCER IS LOCATED AT THE 3' END OF THE MYOSIN LIGHT-CHAIN 1/3 GENE LOCUS, GENES & DEVELOPMENT, Vol: 2, Pages: 1779-1790, ISSN: 0890-9369
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- Citations: 203
ROSENTHAL N, 1987, IDENTIFICATION OF REGULATORY ELEMENTS OF CLONED GENES WITH FUNCTIONAL ASSAYS, METHODS IN ENZYMOLOGY, Vol: 152, Pages: 704-720, ISSN: 0076-6879
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- Citations: 492
ROSENTHAL N, DONOGHUE M, 1987, REGULATION OF RAT MYOSIN LIGHT CHAIN GENES, Publisher: WILEY-LISS, Pages: 89-89, ISSN: 0730-2312
Jacob R, Rosenthal N, Barrett EJ, 1986, Characterization of glutamine transport by liver plasma membrane vesicles., Am J Physiol, Vol: 251, Pages: E509-E514, ISSN: 0002-9513
Plasma membrane vesicles were prepared from livers of fed normal and diabetic rats and used to characterize the membrane transport process responsible for glutamine uptake by the liver cell. In vesicles from normal rats the initial velocity of glutamine uptake was fourfold more rapid (0.20 +/- 0.02 vs. 0.05 +/- 0.02 nmol X mg protein-1 X 10 s-1) when Na+ replaced K+ in the extravesicular buffer. In the presence of a Na+-gradient glutamine uptake by vesicles was saturable, with a Km of 1.3 +/- 0.5 mM and a Vmax of 10 +/- 2.3 nmol X mg-1 X min-1. Lithium could fully substitute for Na+ in stimulating glutamine entry. In the presence of an imposed K+-gradient glutamine uptake was a linear function of its extravesicular concentration. In accord with the sodium-stimulated uptake of glutamine occurring via a sodium symport process, we observed that glutamine stimulated the initial rate of 22Na+ entry into vesicles by four- to fivefold. We further observed that glutamine entry was more rapid when lipophilic anions accompanied sodium in the incubation buffer, suggesting that Na+-glutamine flux is electrogenic. Preloading of vesicles with glutamine did not effect subsequent entry of labeled glutamine (no transstimulation), whereas intravesicular alanine did enhance alanine but not glutamine entry. Alloxan diabetes, which is known to stimulate the Na+-alanine cotransporter in these vesicles did not increase glutamine entry at any concentration tested.(ABSTRACT TRUNCATED AT 250 WORDS)
Rosenthal NR, Jacob R, Barrett E, 1985, Diabetes enhances activity of alanine transport in liver plasma membrane vesicles., Am J Physiol, Vol: 248, Pages: E581-E587, ISSN: 0002-9513
In the present study plasma membrane vesicles were prepared from livers of control and alloxan-induced diabetic rats and the substrate specificity and kinetic characteristics of alanine transport determined in both groups. Sodium-dependent alanine uptake at physiological alanine concentrations (100 microM) was enhanced threefold in diabetic as compared with control animals (0.31 +/- 0.04 vs. 0.11 +/- 0.01 nmol X mg protein-1 X 10 s-1). This accelerated influx corresponded to a three- to fourfold increase in the Vmax of alanine transport in diabetic versus control group (7.1 +/- 2.1 vs. 1.6 +/- 0.2 nmol X mg protein-1 X 10 s-1, P less than 0.05), whereas the Km of alanine uptake was unchanged (2.8 +/- 1.2 vs. 1.4 +/- 0.1 mM). Other neutral amino acids (20 mM) inhibited alanine transport to a similar degree in both groups. The sodium-dependent influx of glutamine (100 microM) was similar in diabetic and control groups (0.17 +/- 0.03 and 0.14 +/- 0.02 nmol X mg protein-1 X 10 s-1, respectively). The initial velocity of 22Na uptake (80 mM) into vesicles and half-maximal stimulation of alanine transport was achieved at essentially identical sodium concentrations (approximately 40 mM) in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
ROSENTHAL N, KRESS M, GRUSS P, et al., 1983, BK VIRAL ENHANCER ELEMENT AND A HUMAN CELLULAR HOMOLOG, SCIENCE, Vol: 222, Pages: 749-755, ISSN: 0036-8075
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- Citations: 146
Lomedico PT, Rosenthal N, Kolodner R, et al., 1980, The structure of rat preproinsulin genes., Ann N Y Acad Sci, Vol: 343, Pages: 425-432, ISSN: 0077-8923
In rat there are two nonallelic insulins, I and II. We have cloned and sequenced double stranded cDNA copies of both preproinsulin mRNA I and II. Using the cloned sequence as probe, we established by the Southern blotting technique a restriction map of the two chromosomal genes. This map indicates that an intron exists within the insulin II gene. To examine this in more detail, we have isolated both genes from a library of rat DNA cloned in phage lambda. Restriction endonuclease analysis and direct DNA sequencing revealed that gene II contains two introns: a 490 base pair intron between the region encoding amino acids 38 and 39 of proinsulin, and a 119 base pair intron, which is 17 base pairs upstream from the initiation codon. Gene I is not interrupted within the protein coding region, but possesses an intron homologous to the 119 base pair intron of insulin II. We are studying the structure of insulin genes from other species to determine if the 490 base pair intron was lost or inserted in the duplicated gene. We have identified nuclear RNA molecules larger than preproinsulin mRNA which contain the transcribed intronic sequences. These molecules represent a new precursor in insulin biosynthesis.
LOMEDICO P, ROSENTHAL N, EFSTRATIADIS A, et al., 1979, STRUCTURE AND EVOLUTION OF THE 2 NONALLELIC RAT PREPROINSULIN GENES, CELL, Vol: 18, Pages: 545-558, ISSN: 0092-8674
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- Citations: 492
JONES CW, ROSENTHAL N, RODAKIS GC, et al., 1979, EVOLUTION OF 2 MAJOR CHORION MULTIGENE FAMILIES AS INFERRED FROM CLONED CDNA AND PROTEIN SEQUENCES, CELL, Vol: 18, Pages: 1317-1332, ISSN: 0092-8674
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- Citations: 85
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