Chang Ge | University of York (original) (raw)

Papers by Chang Ge

Journal of Physics B-atomic Molecular and Optical Physics, 2008

We study the Doppler-broadened absorption of a weak monochromatic probe beam in a thermal rubidiu... more We study the Doppler-broadened absorption of a weak monochromatic probe beam in a thermal rubidium vapour cell on the D lines. A detailed model of the susceptibility is developed which takes into account the absolute linestrengths of the allowed electric dipole transitions and the motion of the atoms parallel to the probe beam. All transitions from both hyperfine levels of the ground term of both isotopes are incorporated. The absorption and refractive index as a function of frequency are expressed in terms of the complementary error function. The absolute absorption profiles are compared with experiment, and are found to be in excellent agreement provided a sufficiently weak probe beam with an intensity under one thousandth of the saturation intensity is used. The importance of hyperfine pumping for open transitions is discussed in the context of achieving the weak-probe limit. Theory and experiment show excellent agreement, with an rms error better than 0.2% for the D2 line at 16.5 degrees C.

Molecular and Cellular Biology, 2000

Oncogenic Src proteins have been extensively studied to gain insight into the signaling mechanism... more Oncogenic Src proteins have been extensively studied to gain insight into the signaling mechanisms of Src. To better understand signaling through wild-type Src, we used an approach that involves activation of Src signaling through the binding of physiologic ligands to the Src SH3 domain. To this end, we used full-length and truncated versions of the multiadapter molecules Cas and Sin to activate c-Src, and we examined the intracellular pathways that mediate Src signaling under these conditions. We show that although all proteins bind to and are phosphorylated by c-Src, quantitative differences exist in the ability of the different ligands to activate c-Src signaling. In addition, we show that Sin-and Cas-induced Src signaling, as assayed by transcriptional activation, is exclusively mediated through a pathway that involves the adapter Crk and the GTP-binding protein Rap1. These data are in contrast to previous observations showing Ras to mediate signaling downstream of transforming Src alleles. In our system, we found that signaling through the oncogenic SrcY527 mutant is indeed mediated by Ras. In addition, we found that Rap1 also mediates oncogenic Src signaling. Our results show for the first time that Rap1 mediates c-Src kinase signaling and reveal mechanistic differences in the signaling properties of wild-type and transforming Src proteins. . † This report is dedicated to the memory of Eugenia Spanopoulou, Andrew Hotchev, and Platon Spanopoulos-Hotchev. ⌬ε ␣ ε. 7363 on December 4, 2013 by guest http://mcb.asm.org/ Downloaded from 7364 XING ET AL. MOL. CELL. BIOL.

Journal of Hypertension, 1999

To investigate whether one kidney one clip (1K-1C) hypertensive rats associated with high levels ... more To investigate whether one kidney one clip (1K-1C) hypertensive rats associated with high levels of angiotensin II (Ang II) exhibit enhanced expression and functions of G proteins in the heart and whether the enhanced expression can be attributed to Ang II. The levels of G protein and G protein mRNA in hearts from 1K-1C hypertensive rats were determined by immunoblotting and Northern blotting techniques using specific antibodies and cDNA probes, respectively, for different isoforms of G proteins. Adenylyl cyclase activity, stimulated or inhibited by agonists, was determined to examine the function of G proteins. The levels of Gialpha-2 and Gialpha-3 proteins and mRNA were significantly increased in hearts from 1K-1C hypertensive rats compared with control rats, whereas the levels of Gsalpha were unchanged. Guanosine 5'-[3'-thio] triphosphate (GTPgammaS), isoproterenol, glucagon, sodium fluoride (NaF) and forskolin (FSK) stimulated adenylyl cyclase activity in hearts from control and hypertensive rats to varying degrees; however, the stimulations were significantly less in hypertensive rats compared with control rats. On the other hand, the inhibitory effect of low concentrations of GTPgammaS on FSK-stimulated adenylyl cyclase activity (an index of Gi function) was significantly enhanced in hearts from 1K-1C hypertensive rats, whereas the inhibitory effect of C-ANF4-23 on adenylyl cyclase was increased and that of Ang II was decreased in hearts from 1K-1C hypertensive rats. Captopril, an angiotensin-converting enzyme inhibitor, restored the augmented levels of Gi proteins and also the altered stimulation and inhibition of adenylyl cyclase by GTPgammaS, stimulatory and inhibitory hormones, respectively, in hearts from hypertensive rats. These data suggest that 1K-1C hypertensive rats exhibit enhanced expression of Gialpha proteins and associated functions that may be attributable to the enhanced levels of Ang II in this model of hypertension.

Archives of Biochemistry and Biophysics, 1999

In the present studies, we have investigated the effect of angiotensin II (AII) on guanine nucleo... more In the present studies, we have investigated the effect of angiotensin II (AII) on guanine nucleotide regulatory protein (G protein) expression and functions in A10 smooth muscle cells. AII treatment of A10 cells enhanced the levels of inhibitory guanine nucleotide regulatory protein (Gi) as well as Gi mRNA and not of stimulatory guanine nucleotide regulatory protein (Gs) in a concentration-dependent manner as determined by immunoblot and Northern blot analysis, respectively. AII-evoked increased expression of Gi␣-2 and Gi␣-3 was inhibited by actinomycin D treatment (RNA synthesis inhibitor). The increased expression of Gi␣-2 and Gi␣-3 by AII was not reflected in functions, because the GTP␥S-mediated inhibition of forskolinstimulated adenylyl cyclase and the receptor-mediated inhibition of adenylyl cyclase by AII and C-ANP 4-23 [des(Gln 18 , Ser 19 , Gln 20 , Leu 21 , Gly 22 ) ANP 4-23 -NH 2 ] were not augmented but attenuated in AIItreated A10 cells. The attenuation was prevented by staurosporine (a protein kinase C inhibitor) treatment. On the other hand, AII treatment did not affect the expression and functions of stimulatory guanine nucleotide regulatory protein (Gs), however, the stimulatory effects of 5-O-(3-thiotriphosphate), isoproterenol, and N-ethylcarboxamide adenosine (NECA) on adenylyl cyclase activity were inhibited to various degrees by AII treatment. Staurosporine reversed the AII-evoked attenuation of isoproterenol-and NECAstimulated enzyme activity. From these results, it can be suggested that AII, whose levels are increased in hypertension, may be one of the possible contributing factors responsible for exhibiting an enhanced expression of Gi protein in hypertension.

Biochemical and Biophysical Research Communications, 1998

To what extent can non-native speaker teachers teach speaking successfully in foreign language le... more To what extent can non-native speaker teachers teach speaking successfully in foreign language learning contexts?

Journal of Physics B-atomic Molecular and Optical Physics, 2008

We study the Doppler-broadened absorption of a weak monochromatic probe beam in a thermal rubidiu... more We study the Doppler-broadened absorption of a weak monochromatic probe beam in a thermal rubidium vapour cell on the D lines. A detailed model of the susceptibility is developed which takes into account the absolute linestrengths of the allowed electric dipole transitions and the motion of the atoms parallel to the probe beam. All transitions from both hyperfine levels of the ground term of both isotopes are incorporated. The absorption and refractive index as a function of frequency are expressed in terms of the complementary error function. The absolute absorption profiles are compared with experiment, and are found to be in excellent agreement provided a sufficiently weak probe beam with an intensity under one thousandth of the saturation intensity is used. The importance of hyperfine pumping for open transitions is discussed in the context of achieving the weak-probe limit. Theory and experiment show excellent agreement, with an rms error better than 0.2% for the D2 line at 16.5 degrees C.

Molecular and Cellular Biology, 2000

Oncogenic Src proteins have been extensively studied to gain insight into the signaling mechanism... more Oncogenic Src proteins have been extensively studied to gain insight into the signaling mechanisms of Src. To better understand signaling through wild-type Src, we used an approach that involves activation of Src signaling through the binding of physiologic ligands to the Src SH3 domain. To this end, we used full-length and truncated versions of the multiadapter molecules Cas and Sin to activate c-Src, and we examined the intracellular pathways that mediate Src signaling under these conditions. We show that although all proteins bind to and are phosphorylated by c-Src, quantitative differences exist in the ability of the different ligands to activate c-Src signaling. In addition, we show that Sin-and Cas-induced Src signaling, as assayed by transcriptional activation, is exclusively mediated through a pathway that involves the adapter Crk and the GTP-binding protein Rap1. These data are in contrast to previous observations showing Ras to mediate signaling downstream of transforming Src alleles. In our system, we found that signaling through the oncogenic SrcY527 mutant is indeed mediated by Ras. In addition, we found that Rap1 also mediates oncogenic Src signaling. Our results show for the first time that Rap1 mediates c-Src kinase signaling and reveal mechanistic differences in the signaling properties of wild-type and transforming Src proteins. . † This report is dedicated to the memory of Eugenia Spanopoulou, Andrew Hotchev, and Platon Spanopoulos-Hotchev. ⌬ε ␣ ε. 7363 on December 4, 2013 by guest http://mcb.asm.org/ Downloaded from 7364 XING ET AL. MOL. CELL. BIOL.

Journal of Hypertension, 1999

To investigate whether one kidney one clip (1K-1C) hypertensive rats associated with high levels ... more To investigate whether one kidney one clip (1K-1C) hypertensive rats associated with high levels of angiotensin II (Ang II) exhibit enhanced expression and functions of G proteins in the heart and whether the enhanced expression can be attributed to Ang II. The levels of G protein and G protein mRNA in hearts from 1K-1C hypertensive rats were determined by immunoblotting and Northern blotting techniques using specific antibodies and cDNA probes, respectively, for different isoforms of G proteins. Adenylyl cyclase activity, stimulated or inhibited by agonists, was determined to examine the function of G proteins. The levels of Gialpha-2 and Gialpha-3 proteins and mRNA were significantly increased in hearts from 1K-1C hypertensive rats compared with control rats, whereas the levels of Gsalpha were unchanged. Guanosine 5'-[3'-thio] triphosphate (GTPgammaS), isoproterenol, glucagon, sodium fluoride (NaF) and forskolin (FSK) stimulated adenylyl cyclase activity in hearts from control and hypertensive rats to varying degrees; however, the stimulations were significantly less in hypertensive rats compared with control rats. On the other hand, the inhibitory effect of low concentrations of GTPgammaS on FSK-stimulated adenylyl cyclase activity (an index of Gi function) was significantly enhanced in hearts from 1K-1C hypertensive rats, whereas the inhibitory effect of C-ANF4-23 on adenylyl cyclase was increased and that of Ang II was decreased in hearts from 1K-1C hypertensive rats. Captopril, an angiotensin-converting enzyme inhibitor, restored the augmented levels of Gi proteins and also the altered stimulation and inhibition of adenylyl cyclase by GTPgammaS, stimulatory and inhibitory hormones, respectively, in hearts from hypertensive rats. These data suggest that 1K-1C hypertensive rats exhibit enhanced expression of Gialpha proteins and associated functions that may be attributable to the enhanced levels of Ang II in this model of hypertension.

Archives of Biochemistry and Biophysics, 1999

In the present studies, we have investigated the effect of angiotensin II (AII) on guanine nucleo... more In the present studies, we have investigated the effect of angiotensin II (AII) on guanine nucleotide regulatory protein (G protein) expression and functions in A10 smooth muscle cells. AII treatment of A10 cells enhanced the levels of inhibitory guanine nucleotide regulatory protein (Gi) as well as Gi mRNA and not of stimulatory guanine nucleotide regulatory protein (Gs) in a concentration-dependent manner as determined by immunoblot and Northern blot analysis, respectively. AII-evoked increased expression of Gi␣-2 and Gi␣-3 was inhibited by actinomycin D treatment (RNA synthesis inhibitor). The increased expression of Gi␣-2 and Gi␣-3 by AII was not reflected in functions, because the GTP␥S-mediated inhibition of forskolinstimulated adenylyl cyclase and the receptor-mediated inhibition of adenylyl cyclase by AII and C-ANP 4-23 [des(Gln 18 , Ser 19 , Gln 20 , Leu 21 , Gly 22 ) ANP 4-23 -NH 2 ] were not augmented but attenuated in AIItreated A10 cells. The attenuation was prevented by staurosporine (a protein kinase C inhibitor) treatment. On the other hand, AII treatment did not affect the expression and functions of stimulatory guanine nucleotide regulatory protein (Gs), however, the stimulatory effects of 5-O-(3-thiotriphosphate), isoproterenol, and N-ethylcarboxamide adenosine (NECA) on adenylyl cyclase activity were inhibited to various degrees by AII treatment. Staurosporine reversed the AII-evoked attenuation of isoproterenol-and NECAstimulated enzyme activity. From these results, it can be suggested that AII, whose levels are increased in hypertension, may be one of the possible contributing factors responsible for exhibiting an enhanced expression of Gi protein in hypertension.

Biochemical and Biophysical Research Communications, 1998

To what extent can non-native speaker teachers teach speaking successfully in foreign language le... more To what extent can non-native speaker teachers teach speaking successfully in foreign language learning contexts?