Biomedical subjects

H Su

Publications and source records attributed to H Su.

At least 109 records · Page 6Linked to original sources

PubMed1995

Early malnutrition followed by nutritional restoration lowers the conduction velocity and excitability of the corticospinal tract.

The physiological sequelae of undernutrition were investigated in rats that were undernourished from day 1-21 and subsequently free-fed to 75 days of age. Population responses were recorded in the corticospinal tract following surface stimulation of the motor cortex, which activates corticospinal cells directly, and also indirectly via cortical synapses. The conduction velocity of the fastest corticospinal fibers in 15 malnourished rats was 16.9 m/s, significantly slower (P < 0.001) than the 20.0 m/s observed in 26 controls. In addition, the excitability of corticospinal neurons to direct stimulation was reduced as much as 67% in malnourished rats, while no effect on synaptic activation was observed. Our findings suggest that early malnutrition reduces the number of large fibers in the adult corticospinal tract. These results are discussed with respect to known morphological and behavioral effects of malnutrition in rats and their relevance to humans.

Analysis of Variance↗

PubMed1995

Molecular mobility of the Ca(2+)-deficient EF-hand of cardiac troponin C as revealed by fluorescence polarization of genetically inserted tryptophan.

To probe attitudinal features of the Ca(2+)-deficient site (site I) in the Ca2+ switch of cardiac troponin C (cTnC), we have examined steady-state fluorescence emission and polarization of a Trp26 inserted in a recombinant cardiac TnC (cTnC3.W) and compared these with the properties of the Ca(2+)-competent site I in skeletal TnC (sTnC4.W). The Ca(2+)-induced fluorescence emission in cTnC3.W was a fraction (25-30%) of that in sTnC4.W, in agreement with previous observations on the Ca(2+)-deficient site incorporated in a cardiac/skeletal chimera c1/s.W [Gulati, J. & Rao, V. G. (1994) Biochemistry 33, 9052-9056]. Thus, the fractional quantum yield reflected intrinsic properties of the cardiac metal ion-deficient site I. Conversely, in sTnC-1.W, where the skeletal site I also was made Ca(2+)-deficient by D27-->A substitution, the Ca(2+)-induced quantum yield was lower than that in cTnC3.W. Nevertheless, similar steady-state fluorescence polarizations for Ca(2+)-saturated sTnC4.W and cTnC3.W indicated indistinguishable final conformations in the two activated TnC isoforms. In EGTA, the polarization parameter (PEGTA) of sTnC4.W is greater than that of cardiac TnC, and the cardiac PEGTA value is closer to the activated PCa. Comparison of the chimera c1/s.W with sTnC-1.W indicated that the differences in conformation of the site I Trp for the EGTA-treated cardiac/skeletal isoforms were due to the structural disparities in this region. This contention was further supported by examination of the chimera CBc1/s.W, where the cardiac EF-hand was altered by 27VLGA30-->DAD substitution. Polarization of the relaxed form was similar to that for sTnC4.W. These findings suggest that the relaxed conformation of the cardiac Ca2+ switch is more favorably predisposed to activation than the skeletal switch.

Animals↗

PubMed1995

Protective efficacy of a parenterally administered MOMP-derived synthetic oligopeptide vaccine in a murine model of Chlamydia trachomatis genital tract infection: serum neutralizing IgG antibodies do not protect against chlamydial genital tract infection.

The protective efficacy of an alum-adsorbed, parenterally administered synthetic oligopeptide immunogen corresponding to antigenically common T-helper and neutralizing B-cell epitopes of the Chlamydia trachomatis major outer membrane protein was studied in a murine model of chlamydial genital tract infection. Mice produced high levels of anti-chlamydial serum IgG neutralizing antibodies following subcutaneous immunization with the alum-adsorbed oligopeptide. Lower but detectable levels of chlamydial specific IgG antibodies were found in vaginal washes. IgG1 was the predominant isotype present in sera and vaginal washes. Chlamydial-specific IgA was not present in either the sera or vaginal washes of immunized mice. Vaccinated and control mice were challenged intravaginally or intrauterinally with low, medium, or high doses of C. trachomatis serovar D challenge inocula. Protection was assessed by performing quantitative chlamydial cervico-vaginal cultures over the course of the infection period. There were no statistically significant differences between groups of immunized and control mice in either colonization, shedding, or duration of infection. These findings demonstrate that parenteral immunization with the oligopeptide (serum-neutralizing antibodies) is ineffective in preventing chlamydial genital tract infection. It is possible, since chlamydial infection is restricted to the genital tract mucosae, that a more accurate evaluation of the oligopeptide vaccine potential will require local rather than systemic immunization.

Administration, Intravaginal↗

PubMed1995

Ovarian morphology and follicular development in sex-linked imperfect albino (s(al)-s) and nonalbino hens before or after a forced moult.

1. The effects of the s(al-s) gene on ovarian morphology and the development of ovarian follicles in old laying hens before and after a forced moult were investigated by measuring and weighing the ovaries and follicles. 2. The laying rate of albinos was higher than that of nonalbinos before the forced moult but not afterwards. Hierarchical follicles in albino hens were smaller than those of nonalbinos before but not after the moult. 3. Growth intensity of hierarchical follicles was greater in albino hens before the moult, suggesting that follicular maturation was more rapid, possibly explaining the higher egg production observed. 4. All differences between genotypes disappeared after the moult, suggesting that the state of the ovary before a moult is independent of that afterwards.

Albinism↗

PubMed1995

Protective efficacy of major outer membrane protein-specific immunoglobulin A (IgA) and IgG monoclonal antibodies in a murine model of Chlamydia trachomatis genital tract infection.

The protective efficacy of immunoglobulin A (IgA) and IgG monoclonal antibodies (MAbs) specific for the major outer membrane protein of Chlamydia trachomatis MoPn was evaluated in a murine genital tract infection model. MAbs were delivered into serum and vaginal secretions of naive mice by using the backpack hybridoma tumor system, and protective efficacy was assessed over the first 8 days following challenge by quantitative determination of chlamydial recovery from cervicovaginal swabs, histopathological evaluation of genital tract tissue, and immunohistochemical detection of chlamydial inclusions. IgA and IgG significantly reduced the incidence of infection following vaginal challenge with 5 50% infectious doses, but such protection was overwhelmed by 10- and 100-fold higher challenge doses. Both MAbs also consistently reduced vaginal shedding from infected animals with all three challenge doses compared with the negative control MAb, although the magnitude of this effect was marginal. Blinded pathological evaluation of genital tract tissues at 8 days postinfection showed a significant reduction in the severity of the inflammatory infiltrate in oviduct tissue of infected IgA- and IgG-treated animals. Immunohistochemical detection of chlamydial inclusions revealed a marked reduction in the chlamydial burden of the oviduct epithelium; this finding is consistent with the reduced pathological changes observed in this tissue. These studies indicate that the presence of IgA or IgG MAbs specific to major outer membrane proteins has a marginal effect in preventing chlamydial colonization and shedding from the genital tract but has a more pronounced effect on ascending chlamydial infection and accompanying upper genital tract pathology.

Animals↗

PubMed1995

Poliovirus hybrids expressing neutralization epitopes from variable domains I and IV of the major outer membrane protein of Chlamydia trachomatis elicit broadly cross-reactive C. trachomatis-neutralizing antibodies.

Trachoma and sexually transmitted diseases caused by Chlamydia trachomatis are major health problems worldwide. Epitopes from the variable domains of the major outer membrane protein are candidates for vaccine development. We have constructed hybrid polioviruses expressing sequences from major outer membrane protein variable domains I and IV. Antisera to the hybrids could, in combination, strongly neutralize 8 of the 12 C. trachomatis serovars most commonly associated with oculogenital infections and weakly neutralize the others.

Amino Acid Sequence↗

PubMed1995

Kinetics of chlamydial antigen processing and presentation to T cells by paraformaldehyde-fixed murine bone marrow-derived macrophages.

Macrophages are potential candidates for antigen presentation to chlamydial-specific CD4+ T cells. We have studied the kinetics of chlamydial antigen processing and presentation by using paraformaldehyde-fixed bone marrow-derived macrophages (BMDM) and splenic T cells isolated from chlamydia-infected mice. BMDM were inoculated with different multiplicities of heat-killed chlamydial elementary bodies, and at different times postingestion, the macrophages were fixed with paraformaldehyde and used as antigen-presenting cells in T-cell proliferation assays. T-cell proliferative responses were shown to be dependent on the chlamydial inoculum size, with a multiplicity of 10 chlamydiae per macrophage producing optimum T-cell proliferation. Temporal experiments showed that peak T-cell proliferative responses occurred between 4 and 12 h postingestion of chlamydiae by BMDM. T cells proliferated strongly to antigen when presented by H-2-matched BMDM but not when presented by H-2-disparate BMDM, demonstrating that T-cell recognition of processed chlamydial antigen was major histocompatibility complex restricted. BMDM inoculated with 10 chlamydiae per cell and fixed at 8 h postinoculation were shown to be as stimulatory to T cells as conventional splenic antigen-presenting cells. Because large numbers of BMDM can be propagated in vitro, and experimental conditions that provide optimum presentation of processed chlamydial antigen to chlamydia-specific CD4+ T cells can be defined, BMDM may be a potentially useful source for the isolation of naturally processed parasite antigen from major histocompatibility complex class II molecules.

Animals↗

PubMed1995

CD4+ T cells play a significant role in adoptive immunity to Chlamydia trachomatis infection of the mouse genital tract.

The ability of CD4+ and CD8+ T cells to adoptively immunize mice against Chlamydia trachomatis infection of the mouse genital tract was studied. Adoptive transfer experiments were performed with splenic CD4+ or CD8+ T cells obtained from mice following resolution of a primary genital tract infection and after a secondary chlamydial challenge. The results show that donor CD4+ T cells, but not CD8+ T cells, obtained from mice following resolution of a primary infection or after secondary challenge were effective in transferring significant antichlamydial immunity to the genital tracts of naive animals. The lymphokine profiles in the culture supernatants of proliferating Chlamydia-specific CD4+ T cells obtained from mice following resolution of a primary infection and after secondary challenge were assayed by an enzyme-linked immunoadsorbent assay. Protective CD4+ T cells restimulated in vitro secreted interleukin 2, gamma interferon, and interleukin 6, lymphokine profiles characteristic of both Th1- and Th2-like responses. Resting CD4+ T cells obtained from mice 4 months following resolution of a primary infection were also capable of conferring significant levels of adoptive protective immunity to naive mice. These findings support an important role for CD4+ T cells in acquired immunity to chlamydial infection of the genital tract and indicate that protective CD4+ immune responses in this model are relatively long lived.

Animals↗

PubMed1994

The number of amino acid residues in hydrophilic loops connecting transmembrane domains of the GABA transporter GAT-1 is critical for its function.

Transporter proteins consist of multiple transmembrane domains connected by hydrophillic loops. As the importance of these loops in transport processes is poorly understood, we have studied this question using the cDNA coding for GAT-1, a Na+/Cl(-)-coupled gamma-aminobutyric acid transporter from rat brain. Deletions of randomly picked non-conserved single amino acids in the loops connecting helices 7 and 8 or 8 and 9 result in inactive transport upon expression in HeLa cells. However, transporters where these amino acids are replaced with glycine retain significant activity. The expression level of the inactive mutant transporters was similar to that of the wild-type, but one of these, delta Val-348, appears to be defectively targetted to the plasma membrane. Our data are compatible with the idea that a minimal length of the loops is required, presumably to enable the transmembrane domains to interact optimally with each other.

Amino Acid Sequence↗

PubMed1994

Disparate contributions of Tyr10 and Tyr109 to fluorescence intensity of rabbit skeletal muscle troponin C identified using a genetically engineered mutant.

Intrinsic tyrosines, as monitored by fluorescence spectroscopy, are sensitive reporters of local, Ca(2+)-induced conformational changes in troponin C (TnC). Rabbit skeletal TnC contains two tyrosines (Y10 in the N-helix, and Y109 in site 3 in the C-terminal domain) in distinct microenvironments: their individual contributions to total fluorescence intensity are elucidated here utilizing bacterially synthesized rabbit skeletal TnC (sTnC4) and a genetically engineered variant, termed 109YF, lacking one of the tyrosines (Y109 replaced with F109). The steady-state fluorescence emission spectra following excitation at 280 nm were recorded in EGTA (Ca(2+)-free) and Ca(2+)-saturated (pCa4) solutions. For the wild-type sTnC4, pCa4 causes a significant (46%) increase in the peak fluorescence intensity over the value in EGTA. For the mutant 109YF, the EGTA fluorescence is only marginally affected (74% of the wild-type FEGTA), but interestingly the Ca2+ effect is completely suppressed (delta F = FpCa4-FEGTA = 2% of the wild-type value). These results indicate that the two tyrosines make disparate contributions to the fluorescence spectrum of wild-type sTnC, both in the presence and absence of Ca2+; whereas Y10 in the N-helix is dominant in Ca(2+)-free solution, Y109 is the sole contributor to the Ca2+ effect. Furthermore, to explain the biphasic fluorescence response of Y109 obtained during Ca2+ titrations, the findings yield the most unequivocal evidence that Ca(2+)-induced conformational changes in the trigger sites operating the contractile switch modify properties of the C-terminal sites in TnC pari passu.

Animals↗

PubMed1994

The human homologue of the retroviral oncogene qin maps to chromosome 14q13.

Chromosomal mapping of the human QIN gene (renamed FKH2 by the Human Genome Organization Nomenclature Committee) was initially accomplished by correlation of the presence of the QIN locus with specific chromosome regions in a rodent-human hybrid panel. This analysis revealed that the human QIN gene maps to chromosome region 14q11.2-->14q32, between the TCR and IGH loci. Further analysis by fluorescence in situ hybridization techniques with a human QIN genomic clone refined the human QIN gene localization to 14q13.

Chromosome Mapping↗

PubMed1994

The role of glycine (residue 89) in the central helix of EF-hand protein troponin-C exposed following amino-terminal alpha-helix deletion.

Because an N-terminal alpha-helical (N-helix) arm and a KGK-triplet (residues 88KGK90) in the central helix of troponin-C (TnC) are missing in calmodulin, several recent studies have attempted to elucidate the structure-function correlations of these units. Presently, with a family of genetically manipulated derivatives especially developed for this study and tested on permeabilized isolated single skeletal muscle fiber segments, we explored the specificities of the amino acid residues within the N-helix and the KGK-triplet in TnC. Noticeably, the amino acid compositions vary between the N-helices of the cardiac and skeletal TnC isoforms. On the other hand, the KGK-triplet is located similarly in both TnC isoforms. We previously indicated that deletion of the N-helix (mutant delta Nt) diminishes the tension obtained on activation with maximal calcium, but the contractile function is revived by the superimposed deletion of the 88KGK90-triplet (mutant delta Nt delta KGK; see Gulati J, Babu A, Su H, Zhang YF, 1993, J Biol Chem 268:11685-11690). Using this functional test, we find that replacement of Gly-89 with a Leu or an Ala could also overcome the contractile defect associated with N-helix deletion. On the other hand, replacement of the skeletal TnC N-helix with cardiac type N-helix was unable to restore contractile function. The findings indicate a destabilizing influence of Gly-89 residue in skeletal TnC and suggest that the N-terminal arm in normal TnC serves to moderate this effect. Moreover, specificity of the N-helix between cardiac and skeletal TnCs raises the possibility that resultant structural disparities are also important for the functional distinctions of the TnC isoforms.

Amino Acid Sequence↗

PubMed1994

Development of polyclonal antibodies and evaluation of a sensitive radioimmunoassay for detection and measurement of synaptophysin.

Polyclonal antibodies directed towards synaptophysin were raised against a synthesised peptide corresponding to amino acids 246 to 260 of the human synaptophysin sequence. The antibodies, when applied for immunocytochemical staining, showed a staining pattern identical to that of the commercially available monoclonal antibody SY-38. A radioimmunoassay for measurements of synaptophysin was developed using these antibodies and the peptide as standard and tracer. The radioimmunoassay was used for optimising the conditions for purification of synaptophysin from rat brain. No synaptophysin was detected in blood plasma in humans, not even during an embolisation treatment of tumour metastases in the liver, which induced tumour cell necrosis, in a patient with carcinoid tumours. By radioimmunoassay, synaptophysin was detected in cell homogenate from the PC-12 (160 ng/mg) and LCC-18 (40 ng/mg) cell lines and in the cell culture media. In the LCC-18 cell line the synaptophysin immunoreactivity was found in the plasma membrane, and the presence of synaptophysin was confirmed both by radioimmunoassay measurements and by the Northern blot technique. These data indicate that measurements of synaptophysin using this radioimmunoassay are reliable and that the assay can serve as a useful tool in further explorations of the biological effects of synaptophysin.

Animals↗

PubMed1994

Cardiac myocyte function and left ventricular strains after brief ischemia and reperfusion in rabbits.

BACKGROUND: After a brief episode of ischemia, myocardial function may be depressed for prolonged periods despite reperfusion. The mechanisms of postischemic dysfunction differ depending on the experimental model. Regional ischemia and reperfusion in the intact animal provide a clinically relevant model, but experimental variables are difficult to control. Experimental conditions can be well controlled in isolated cardiac muscle and myocyte preparations, but these models are limited by the assumptions used to mimic ischemia and reperfusion. This study combines the unique advantages of both preparations. We characterized in vivo alterations in regional two-dimensional finite strains with ischemia and reperfusion produced in the intact animal, then isolated cardiac myocytes from the region with postischemic dysfunction to characterize in vitro function of postischemic myocytes. METHODS AND RESULTS: In seven anesthetized rabbits, three piezoelectric crystals were inserted in a triangular array to measure two-dimensional finite strains around the large coronary artery in the left ventricular anterior free wall. After 15 minutes of ischemia and reperfusion, strains were depressed at a stable level approximately 30% to 40% below control values between 1 and 6 hours after reperfusion. The direction of maximal shortening deformations was midway between circumferential and longitudinal directions during control and did not shift after reperfusion. In a second group of five rabbits, cardiac myocytes were isolated from the region with postischemic dysfunction after 15 minutes of ischemia and 45 minutes of reperfusion. We compared in vitro function in 45 postischemic myocytes with 48 cardiac myocytes isolated from five normal rabbits. Each rabbit (postischemic and control) contributed 9 +/- 1 (SD) myocytes to the study. All myocytes were studied within 1 hour after myocyte isolation (approximately 3 to 5 hours after reperfusion for postischemic myocytes). Myocytes were stimulated at 0.5 Hz and perfused with 2 mmol/L [Ca2+] Tyrode's solution to measure unloaded cell shortening. There was significantly less shortening in postischemic myocytes (12.4 +/- 2.1%) than control myocytes (16.2 +/- 1.2%). Maximal cell length (Lmax) was significantly longer in postischemic (134 +/- 7 microns) than control myocytes (122 +/- 7 microns), as was minimum cell length (Lmin) (118 +/- 8 versus 103 +/- 9 microns, respectively). The duration of shortening (time from stimulation to Lmin) was significantly shorter in postischemic (279 +/- 56 milliseconds) than control myocytes (405 +/- 44 milliseconds). Peak rates of cell shortening (-dL/dt) and lengthening (+dL/dt) did not differ. CONCLUSIONS: In rabbits, 15 minutes of ischemia produced a stable depression in finite strains for 1 to 6 hours after reperfusion, with shortening deformations reduced by approximately 30% to 40% without a shift in direction. Cardiac myocytes isolated from postischemic myocardium display functional impairments in vitro similar to those measured in vivo, with an approximately 25% reduction in unloaded myocyte shortening and decreased contraction duration. This indicates that ischemia and reperfusion induce intrinsic impairments in contractility independently of external loading conditions. This model may be useful for examining cellular mechanisms of postischemic myocardial dysfunction.

Animals↗

PubMed1994

Production and quality of eggs from sex-linked imperfect albino (sal-s) and nonalbino (s+) hens kept under commercial conditions.

The beneficial effects of the gene for imperfect albinism on egg production were investigated under commercial conditions. In one line (Line 8) but not in another (Line 3), hen-day egg production of albinos from 46 to 75 wk of age was higher than that of nonalbinos (76.1 vs 72.6%) resulting in higher overall hen-day (71.1 vs 69.3%, P < .08) and hen-housed (276.3 vs 263.6 eggs) egg production by albino hens. Egg production of Line 8 albinos was not different than that of one of two commercial strains (Strain A) included as a control (76.1 vs 75.6%, P > .05). In data from Lines 3 and 8 combined, sexual maturity of albinos was delayed by 3.0 d. Mortality was higher for albinos than nonalbinos (3.6 vs 1.8%) during the first 2 wk of brooding and lower for albinos (5.8 vs 8.9%) during the laying period. Eggs from albinos weighed less (53.8 vs 55.3 g), had smaller yolks (16.9 vs 17.6 g) and shells (5.16 vs 5.27 g), and firmer albumen (5.9 vs 5.6 mm). The results suggest that the gene produces beneficial effects on egg production under commercial conditions.

Albinism↗

PubMed1994

[The influence of obliteration of external lymphatic space on the vestibule and the cochlea in guinea pigs].

Obliteration of the external lymphatic space on 18 guinea pigs was performed. The lymphatic space of the horizontal semicircular canal was blocked by fascia. Auditory (ABR) and vestibular functions were tested before and after the surgical obliteration. Morphologic changes in the cochlea and vestibule were observed under light microscope. It was found that there was no significant difference in the threshold of ABR before and after the operation. However, the sustained time of nystagmus was significantly decreased after the operation. Our results indicate that this surgical procedure may damage vestibular function, but produce no evident damage to the cochlear function.

Animals↗

PubMed1993

Critical minimum length of the central helix in troponin C for the Ca2+ switch in muscular contraction.

In the troponin C (TnC) dumbbell, the NH2- and COOH-terminal lobes are well delineated, but the role of the central helix and especially the function of its long length remain doubtful. To study this, we used a cDNA construct encoding rabbit fast-twitch muscle TnC, comprising multiple restriction sequences to facilitate mutagenesis (Babu, A., Su, H., Ryu, Y. & Gulati, J. (1992) J. Biol. Chem. 267, 15469-15474). Systematically, we have deleted 3-12 amino acid residues from the central helix and examined their effects in maximally activated skinned muscle fibers. Limiting the deletions to 7 amino acid residues manifested little change in maximal force development (Sheng, Z., Francois, J. M., Hitchcock, S. E. & Potter, J. D. (1991) J. Biol. Chem. 266, 5711-5715). However, with further deletions, we now find that contractility was inhibited pari passu; by 12 deletions, the inhibition was complete. The critical minimum length for the central helix is thereby estimated as 27 A. The Ca2+ binding capacity (4 mol of Ca2+/mol of protein) as well as the structural characteristics (alpha-helicity by CD measurements and the fluorescence emitted by Tyr-109) indicated a well preserved global conformation of the short mutant. However, surprisingly, two of these short mutants filled each TnC slot under highly specific superloading conditions: one short molecule was taken up in EGTA solution, and the second molecule was captured and retained with Ca2+. They also rescued the contractile switch, evidently in a bimolecular reaction. Another short variant (putative skeletal fast muscle TnC-I-II), in which the NH2-terminal Ca(2+)-binding sites were incapacitated, failed to respond to superloading, indicating that sites III and IV could not substitute for sites I and II. The results suggest that a critical role of the central helix linker in TnC is to keep the two lobes optimally apart, evidently in proximity of their respective target sites on troponin I in the fiber.

Amino Acid Sequence↗

PubMed1993

Identification of the regions conferring calmodulin-like properties to troponin C.

The structural and functional correlations between troponin C (TnC) and calmodulin (CaM) were investigated by mutagenizing a synthetic cDNA coding rabbit skeletal muscle TnC. Compared with TnC, calmodulin lacks the N-terminal alpha-helical arm (N-helix), and its central helix is shorter due to the absence of 88KGK90 residues. Deleting both regions concomitantly (delta Nt delta KGK) elicited CaM-like regulation as tested (i) by smooth muscle contractility (maximal tension = 80 +/- 5% Po of control) and (ii) by the activation of phosphodiesterase (Vmax = 75 +/- 2% of control). The Ca(2+)-binding capacity of the mutant and the effect of the mutant on maximally Ca(2+)-activated tension of skinned rabbit psoas muscle fibers were both conserved. Furthermore, in the linker region of the central helix, replacing the TnC-characteristic 85EDAKGK90 successive residues with CaM-specific DTD residues generated a highly effective CaM mimic (Vmax = 96 +/- 2%) whether or not the N-helix was also retained. Apparent KD values (i.e. concentrations for half-maximal response) for the successful mutants were similar to each other but about 200-fold higher than that for CaM. A part of the alpha-helical linker region in CaM may unfold and bend to promote multiplicity of target interaction using all four hands (Ikura, M., Clore, G. M., Gronenborn, A. M., Zhu, G., Klee, C. B., and Bax, A. (1992) Science 256, 632-638; Meador, W. E., Means, A. R., and Quiocho, F. A. (1992) Science 257, 1251-1255). In contrast, our results suggest that the TnC central helix evolved to be less pliable by the combined influences of 85EDAKGK90 residues and the alpha-helical extension in N terminus, thereby keeping the N-terminal hands well separated from their C-terminal counterparts.

Amino Acid Sequence↗