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1
Buenafe, A. C., R. C. Tsu, B. Bebo, A. C. Bakke, A. A. Vandenbark, and H. Offner. "A TCR V alpha CDR3-specific motif associated with Lewis rat autoimmune encephalomyelitis and basic protein-specific T cell clones." Journal of Immunology 158, no. 11 (June 1, 1997): 5472–83. http://dx.doi.org/10.4049/jimmunol.158.11.5472.
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Abstract To investigate TCR V alpha gene expression in the Lewis rat model of experimental autoimmune encephalomyelitis, we obtained V alpha chain sequences from two V beta8.2+-encephalitogenic, BP72-89-specific T cell clones. Two different V alpha genes, a V alpha2 gene and a V alpha23 gene, are utilized, but both were found to contain an asparagine repeat (Asn3+) sequence present in the V alpha CDR3 region. This Asn3+ motif is also present in the previously reported sequence of a BP68-88-specific hybridoma, 510, which utilizes a different V alpha2 gene family member. In further experiments, spinal cord T cells were isolated at the onset of basic protein (BP)-induced disease and sorted for the OX-40 activation marker, which we have previously used to enrich for specifically activated T cells. Analysis of V alpha expression in the OX-40+ population revealed the biased use of three V alpha genes, V alpha1, V alpha2, and V alpha23. The Asn3+ motif was present in the V alpha CDR3 region of V alpha1, V alpha2, and V alpha23 cDNA derived from OX-40+ spinal cord T cells but found to be generally absent in the OX-40- spinal cord population. Since these Asn3+ motif-bearing V alpha chain sequences are nearly identical to those utilized by the BP-specific encephalitogenic clones described, it is likely that these V alpha sequences are derived from disease-associated T cells in the spinal cord. Thus, we demonstrate that the Asn3+ V alpha CDR3 motif is strongly associated with experimental autoimmune encephalomyelitis in the Lewis rat and propose that it plays a role in TCR recognition of a specific BP peptide/MHC complex.
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Harashima, S., A. M. Miller, K. Tanaka, K. Kusumoto, K. Tanaka, Y. Mukai, K. Nasmyth, and Y. Oshima. "Mating-type control in Saccharomyces cerevisiae: isolation and characterization of mutants defective in repression by a1-alpha 2." Molecular and Cellular Biology 9, no. 10 (October 1989): 4523–30. http://dx.doi.org/10.1128/mcb.9.10.4523-4530.1989.
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The alpha 2 protein, the product of the MAT alpha 2 cistron, represses various genes specific to the a mating type (alpha 2 repression), and when combined with the MATa1 gene product, it represses MAT alpha 1 and various haploid-specific genes (a1-alpha 2 repression). One target of a1-alpha 2 repression is RME1, which is a negative regulator of a/alpha-specific genes. We have isolated 13 recessive mutants whose a1-alpha 2 repression is defective but which retain alpha 2 repression in a genetic background of ho MATa HML alpha HMRa sir3 or ho MAT alpha HMRa HMRa sir3. These mutations can be divided into three different classes. One class contains a missense mutation, designated hml alpha 2-102, in the alpha 2 cistron of HML, and another class contains two mat alpha 2-202, in the MAT alpha locus. These three mutants each have an amino acid substitution of tyrosine or acid substitution of tyrosine or phenylalanine for cysteine at the 33rd codon from the translation initiation codon in the alpha 2 cistron of HML alpha or MAT alpha. The remaining 10 mutants make up the third class and form a single complementation group, having mutations designated aar1 (a1-alpha 2 repression), at a gene other than MAT, HML, HMR, RME1, or the four SIR genes. Although a diploid cell homozygous for the aarl and sir3 mutations and for the MATa, HML alpha, and HMRa alleles showed alpha mating type, it could sporulate and gave rise to asci containing four alpha mating-type spores. These facts indicate that the domain for alpha2 repression is separable from that for a1-alpha2 protein interaction or complex formation in the alpha2 protein and that an additional regulation gene, AAR1, is associated with the a1-alpha2 repression of the alpha1 cistron and haploid-specific genes.
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Harashima, S., A. M. Miller, K. Tanaka, K. Kusumoto, K. Tanaka, Y. Mukai, K. Nasmyth, and Y. Oshima. "Mating-type control in Saccharomyces cerevisiae: isolation and characterization of mutants defective in repression by a1-alpha 2." Molecular and Cellular Biology 9, no. 10 (October 1989): 4523–30. http://dx.doi.org/10.1128/mcb.9.10.4523.
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The alpha 2 protein, the product of the MAT alpha 2 cistron, represses various genes specific to the a mating type (alpha 2 repression), and when combined with the MATa1 gene product, it represses MAT alpha 1 and various haploid-specific genes (a1-alpha 2 repression). One target of a1-alpha 2 repression is RME1, which is a negative regulator of a/alpha-specific genes. We have isolated 13 recessive mutants whose a1-alpha 2 repression is defective but which retain alpha 2 repression in a genetic background of ho MATa HML alpha HMRa sir3 or ho MAT alpha HMRa HMRa sir3. These mutations can be divided into three different classes. One class contains a missense mutation, designated hml alpha 2-102, in the alpha 2 cistron of HML, and another class contains two mat alpha 2-202, in the MAT alpha locus. These three mutants each have an amino acid substitution of tyrosine or acid substitution of tyrosine or phenylalanine for cysteine at the 33rd codon from the translation initiation codon in the alpha 2 cistron of HML alpha or MAT alpha. The remaining 10 mutants make up the third class and form a single complementation group, having mutations designated aar1 (a1-alpha 2 repression), at a gene other than MAT, HML, HMR, RME1, or the four SIR genes. Although a diploid cell homozygous for the aarl and sir3 mutations and for the MATa, HML alpha, and HMRa alleles showed alpha mating type, it could sporulate and gave rise to asci containing four alpha mating-type spores. These facts indicate that the domain for alpha2 repression is separable from that for a1-alpha2 protein interaction or complex formation in the alpha2 protein and that an additional regulation gene, AAR1, is associated with the a1-alpha2 repression of the alpha1 cistron and haploid-specific genes.
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de Bairros, Thiago, Pedro Pereira, Rausley de Souza, and Michel Yacoub. "Bivariate Complex $\alpha$-$\mu$ Statistics." IEEE Transactions on Vehicular Technology 71, no. 3 (March 2022): 3276–80. http://dx.doi.org/10.1109/tvt.2022.3141232.
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REX SHEU, KWAN-FU, and JOHN P. BLASS. "The alpha-Ketoglutarate Dehydrogenase Complex." Annals of the New York Academy of Sciences 893, no. 1 OXIDATIVE/ENE (November 1999): 61–78. http://dx.doi.org/10.1111/j.1749-6632.1999.tb07818.x.
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Pashaei, Ronak, Amir Pishkoo, Mohammad Sadegh Asgari, and Davood Ebrahimi Bagha. "$\alpha$-Differentiable functions in complex plane." Вестник Самарского государственного технического университета. Серия «Физико-математические науки» 24, no. 2 (2020): 379–89. http://dx.doi.org/10.14498/vsgtu1734.
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В комплексной плоскости вводится взвешенная дробная производная порядка $\alpha$. Относительно многозначной функции $ z ^ {1- \alpha} $ получены дробные уравнения Коши-Римана, которые при $ \alpha = 1 $ совпадают с классическими уравнениями Коши-Римана. Для некоторых функций в комплексной плоскости рассмотрены свойства, относящиеся к комплексной взвешенной дробной производной. Обсуждаются два комплексных дифференциальных уравнения специальной формы. Для некоторых значений $\alpha$ приводятся римановы поверхности их решений и сравниваются их графики.
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Moretti, D. V., A. Prestia, G. Binetti, O. Zanetti, and G. B. Frisoni. "Alpha and Theta EEG Rhythms Activity Reveal Deep Changes in Resting Brain State in Subjects with Prodromal Alzheimer's Disease." Journal of Aging and Gerontology 2, no. 1 (February 5, 2014): 13–23. http://dx.doi.org/10.12974/2309-6128.2014.02.01.3.
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The increase of EEG alpha3/alpha2 frequency power ratio has been associated with AD-converters subjects with mild cognitive impairment (MCI) as well as a reduction in the regional cerebral blood flow (rCBF). In this study, the association between alpha3/alpha2 frequency power ratio with rCBF changes in subjects with MCI was evaluated. The alpha3/alpha2 frequency power ratio was computed in 27 subjects with MCI. Two groups were obtained according to the median values of alpha3/alpha2, at a cut-off of 1.17. In the groups so obtained, the correlation between brain perfusion and EEG markers were detected. In the MCI group with the alpha3/alpha2 frequency power ratio above 1,17 as compared to the group with alpha3/alpha2 frequency power ratio below 1.17 there was: 1) a constant trend to lower rCBF values; 2) smaller hippocampal volumes; 3) higher theta frequency power. The higher EEG alpha3 /alpha2 frequency power ratio individuates two different group of MCI subjects. A complex interplay between alpha and theta rhythms activity MCI patients is suggested in patients with prodromal Alzheimer's disease.
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Forster, B., R. Garunkštis, P. Massopust, and J. Steuding. "Complex B-splines and Hurwitz zeta functions." LMS Journal of Computation and Mathematics 16 (2013): 61–77. http://dx.doi.org/10.1112/s146115701300003x.
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AbstractWe characterize nonempty open subsets of the complex plane where the sum $\zeta (s, \alpha )+ {e}^{\pm i\pi s} \hspace{0.167em} \zeta (s, 1- \alpha )$ of Hurwitz zeta functions has no zeros in $s$ for all $0\leq \alpha \leq 1$. This problem is motivated by the construction of fundamental cardinal splines of complex order $s$.
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KUROKAWA, CHIE, and KIYOSHI KATŌ. "THREE-ALPHA STRUCTURES AND ALPHA-CONDENSATION IN 12C." Modern Physics Letters A 18, no. 02n06 (February 28, 2003): 162–65. http://dx.doi.org/10.1142/s0217732303010168.
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The 3α resonances in 12 C are investigated in a framework of the complex scaling method. Calculated resonance parameters well reproduce the experimental data and we can obtain the second 2+ state just above the third 0+ state.
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Green, Colin P., and Peter Osborne. "ALPHA-ACID-1,2-DIAMINOBENZENE COMPLEX: A CONVENIENT STANDARD FOR ALPHA-ACID ANALYSIS." Journal of the Institute of Brewing 99, no. 4 (July 8, 1993): 347–48. http://dx.doi.org/10.1002/j.2050-0416.1993.tb01174.x.
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Falkenberg, C., J. J. Enghild, I. B. Thøgersen, G. Salvesen, and B. Akerström. "Isolation and characterization of fibronectin-α1-microglobulin complex in rat plasma." Biochemical Journal 301, no. 3 (August 1, 1994): 745–51. http://dx.doi.org/10.1042/bj3010745.
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Molecules containing the 28 kDa immunoregulatory protein alpha 1-microglobulin (alpha 1-m), also known as protein HC, were isolated from rat plasma or serum by immunoaffinity chromatography. Three molecular species were distinguished on the basis of nondenaturing PAGE. Two of these have been described previously: uncomplexed alpha 1-m, and the complex of alpha 1-m with alpha 1-inhibitor-3. The third species was analysed by denaturing PAGE, immunoblotting, proteinase digestion and N-terminal-sequence analyses, and shown to consist of a complex between alpha 1-m and fibronectin. This complex, with a mass of about 560 kDa, was resistant to dissociation in the presence of denaturants, but not in the presence of reducing agents in combination with denaturants, and we conclude that the two components are linked by disulphide bonds. About 60% of the total detectable plasma alpha 1-m exists as high-molecular-mass complexes distributed approximately evenly between fibronectin and alpha 1-inhibitor-3. Immunochemical analyses were used to determine the proportion of the total plasma pools of fibronectin and alpha 1-inhibitor-3 that circulate in complex with alpha 1-m. About 3-7% of the total plasma fibronectin from three different rat strains contained alpha 1-m, whereas 0.3-0.8% of the total plasma alpha 1-inhibitor-3 contained alpha 1-m. Complexes were found at similar levels in plasma and serum, indicating that coagulation is not responsible for complex formation. Moreover, immunochemical analyses of human plasma revealed small amounts of alpha 1-m in complex with fibronectin and alpha 2-macroglobulin (an alpha 1-inhibitor-3 homologue). The existence of a complex between alpha 1-m and fibronectin in rats and humans suggests a mechanism for the incorporation of the immunoregulatory molecule alpha 1-m into the extracellular matrix.
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Clancy, Fiona. "Motherhood in crisis in Lucrecia Martel’s Salta Trilogy." Alphaville: Journal of Film and Screen Media, no. 10 (December 16, 2015): 64–75. http://dx.doi.org/10.33178/alpha.10.04.
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This article concerns the complex negotiation of ageing and femininity in Amy Heckerling’s two most recent films: I Could Never Be Your Woman (2007) and Vamps (2012). These films are positioned as part of the contemporary postfeminist media culture, (Gill, 2007) noting the scrutiny received by the ageing female body, and its changing status under the prevailing cultural norms of femininity. However, Heckerling’s films also demonstrate a sense of play with these gender norms, and so calls to be read also in terms of Judith Butler’s theorisation of performativity (1990; 1993; 2004). This article contends that Heckerling’s representation of liminality and indeterminacy—in her teen movies, and later work alike—provides a way for women to carve out an autonomous identity that humorously demonstrates the absurdity of mediatised constructions of femininity. Her work, then, is more complex than has hitherto been acknowledged, and the piece concludes by calling for the director and screenwriter to be repositioned as a significant female voice in 21st century screen media.
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Kim, MinKyung, and UnCheol Lee. "Alpha oscillation, criticality, and responsiveness in complex brain networks." Network Neuroscience 4, no. 1 (January 2020): 155–73. http://dx.doi.org/10.1162/netn_a_00113.
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Brains in unconsciousness are characterized by significantly limited responsiveness to stimuli. Even during conscious wakefulness, responsiveness is highly dependent on ongoing brain activity, specifically, of alpha oscillations (∼10 Hz). We hypothesized that the variety of brain responses to external stimuli result from the interaction between state-specific and transient alpha oscillations and stimuli. To justify this hypothesis, we simulated various alpha oscillations in the human brain network, modulating criticality (a balanced state between order and disorder), and investigated specific alpha oscillation properties (instantaneous amplitude, phase, and global synchronization) that induce a large or small response. As a result, we found that the alpha oscillations near a critical state show a more complex and long-lasting response, which is more prominent when stimuli are given to globally desynchronized and low-amplitude oscillations. We also found specific phases of alpha oscillation that barely respond to stimuli, which implies the presence of temporal windows in the alpha cycle for a large or small response. The results explain why brain responses are so variable across conscious and unconscious states and across time windows even during conscious wakefulness, and emphasize the importance of considering ongoing alpha oscillations for effective brain stimulation.
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Tatit, Luiz. "Transforming Brazilian speech into popular song." Alphaville: Journal of Film and Screen Media, no. 19 (July 23, 2020): 132–38. http://dx.doi.org/10.33178/alpha.19.10.
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In this interview, Luiz Tatit explores some specificities of Brazilian popular song which may explain the considerable success of music documentaries in the country. Such specificities include the connection between popular song and daily speech, its ties with Brazilian national identity and its complex relationship with foreign music styles.
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Tartas, Adrianna, Lovisa Lundholm, Harry Scherthan, Andrzej Wojcik, and Beata Brzozowska. "The order of sequential exposure of U2OS cells to gamma and alpha radiation influences the formation and decay dynamics of NBS1 foci." PLOS ONE 18, no. 6 (June 12, 2023): e0286902. http://dx.doi.org/10.1371/journal.pone.0286902.
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DNA double strand breaks (DSBs) are a deleterious form of DNA damage. Densely ionising alpha radiation predominantly induces complex DSBs and sparsely ionising gamma radiation—simple DSBs. We have shown that alphas and gammas, when applied simultaneously, interact in producing a higher DNA damage response (DDR) than predicted by additivity. The mechanisms of the interaction remain obscure. The present study aimed at testing whether the sequence of exposure to alphas and gammas has an impact on the DDR, visualised by live NBS1-GFP (green fluorescent protein) focus dynamics in U2OS cells. Focus formation, decay, intensity and mobility were analysed up to 5 h post exposure. Focus frequencies directly after sequential alpha → gamma and gamma → alpha exposure were similar to gamma alone, but gamma → alpha foci quickly declined below the expected values. Focus intensities and areas following alpha alone and alpha → gamma were larger than after gamma alone and gamma → alpha. Focus movement was most strongly attenuated by alpha → gamma. Overall, sequential alpha → gamma exposure induced the strongest change in characteristics and dynamics of NBS1-GFP foci. Possible explanation is that activation of the DDR is stronger when alpha-induced DNA damage precedes gamma-induced DNA damage.
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Dragomir, S. S. "New Inequalities of CBS-Type for Power Series of Complex Numbers." Fasciculi Mathematici 57, no. 1 (December 1, 2016): 37–51. http://dx.doi.org/10.1515/fascmath-2016-0015.
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Abstract Let $f(\lambda ) = \sum\nolimits_{n = 0}^\infty {a_n \lambda ^n } $ be a function defined by power series with complex coefficients and convergent on the open disk D(0, R) ⊂ ℂ, R > 0. In this paper we show amongst other that, if α, z ∈ ℂ are such that |α|, |α| |z|2 < R, then $$\left| {f(\alpha )f(\alpha z^2 ) - f^2 (\alpha z)} \right| \le f_A \left( {\left| \alpha \right|} \right) f_A \left( {\left| \alpha \right|\left| z \right|^2 } \right) - \left| {f_A (\left| \alpha \right|z)} \right|^2 .$$ where $f_A (z) = \sum\nolimits_{n = 0}^\infty {\left| {\alpha _n } \right|z^n } $ . Applications for some fundamental functions defined by power series are also provided.
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HOFFMAN, H. DU P., P. R. DONALD, C. HANEKOM, and F. C. DE BEER. "Cerebrospinal fluid alpha-1-antitrypsin alpha-1-antitrypsin-elastase complex levels in meningitis." European Journal of Clinical Investigation 19, no. 1 (January 1989): 26–29. http://dx.doi.org/10.1111/j.1365-2362.1989.tb00191.x.
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HOFFMAN, H. DU P., P. R. DONALD, C. HANEKOM, and F. C. DE BEER. "Cerebrospinal fluid alpha-1-antitrypsin alpha-1-antitrypsin-elastase complex levels in meningitis." European Journal of Clinical Investigation 19, s1 (October 1989): 26–29. http://dx.doi.org/10.1111/j.1365-2362.1989.tb00302.x.
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Banda, M. J., A. G. Rice, G. L. Griffin, and R. M. Senior. "The inhibitory complex of human alpha 1-proteinase inhibitor and human leukocyte elastase is a neutrophil chemoattractant." Journal of Experimental Medicine 167, no. 5 (May 1, 1988): 1608–15. http://dx.doi.org/10.1084/jem.167.5.1608.
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An inhibitor-proteinase complex consisting of human alpha 1-PI and human leukocyte elastase is chemotactic for human neutrophils. The chemotactic activity is optimal at 1 nM and is associated only with the alpha 1-PI portion of the complex. Neither HLE in the complex, free HLE, nor native alpha 1-PI possesses chemotactic activity for human neutrophils. alpha 1-PI in complex is hydrolyzed at the Met-358-Ser-359 bond. The chemotactic activity is associated with the Mr 4,200 fragment of alpha 1-PI that has Ser-359 as its NH2 terminus. The region of the HLE-alpha 1-PI complex that stimulates chemotaxis appears to be the same as that of the Mr 4,200 fragment generated by hydrolysis of the Pro-357-Met-358 bond during proteolytic inactivation of alpha 1-PI. The data suggest the presence of a neutrophil surface receptor bound by alpha 1-PI after the formation of a complex with HLE or after proteolytic degradation. This receptor may play a role in clearance of these modified alpha 1-PI molecules.
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Al-Sharoa, Doaa. "(α1, 2, β1, 2)-complex intuitionistic fuzzy subgroups and its algebraic structure." AIMS Mathematics 8, no. 4 (2023): 8082–116. http://dx.doi.org/10.3934/math.2023409.
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<abstract> <p>A complex intuitionistic fuzzy set is a generalization framework to characterize several applications in decision making, pattern recognition, engineering, and other fields. This set is considered more fitting and coverable to Intuitionistic Fuzzy Sets (IDS) and complex fuzzy sets. In this paper, the abstraction of (${{\alpha _{1, 2}}, {\beta _{1, 2}}}$) complex intuitionistic fuzzy sets and (${{\alpha _{1, 2}}, {\beta _{1, 2}}}$)-complex intuitionistic fuzzy subgroups were introduced regarding to the concept of complex intuitionistic fuzzy sets. Besides, we show that (${{\alpha _{1, 2}}, {\beta _{1, 2}}}$)-complex intuitionistic fuzzy subgroup is a general form of every complex intuitionistic fuzzy subgroup. Also, each of (${{\alpha _{1, 2}}, {\beta _{1, 2}}}$)-complex intuitionistic fuzzy normal subgroups and cosets are defined and studied their relationship in the sense of the commutator of groups and the conjugate classes of group, respectively. Furthermore, some theorems connected the (${{\alpha _{1, 2}}, {\beta _{1, 2}}}$)-complex intuitionistic fuzzy subgroup of the classical quotient group and the set of all (${{\alpha _{1, 2}}, {\beta _{1, 2}}}$)-complex intuitionistic fuzzy cosets were studied and proved. Additionally, we expand the index and Lagrange's theorem to be suitable under (${{\alpha _{1, 2}}, {\beta _{1, 2}}}$)-complex intuitionistic fuzzy subgroups.</p> </abstract>
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Lashin, A. Y. "Convolution conditions for bounded \(\alpha\)-starlike functions of complex order." Annales Universitatis Mariae Curie-Sklodowska, sectio A – Mathematica 71, no. 1 (June 30, 2017): 65. http://dx.doi.org/10.17951/a.2017.71.1.65.
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Let \(A\) be the class of analytic functions in the unit disc \(U\) of the complex plane \(\mathbb{C}\) with the normalization \(f(0)=f^{^{\prime }}(0)-1=0\). We introduce a subclass \(S_{M}^{\ast }(\alpha ,b)\) of \(A\), which unifies the classes of bounded starlike and convex functions of complex order. Making use of Salagean operator, a more general class \(S_{M}^{\ast }(n,\alpha ,b)\) (\(n\geq 0\)) related to \(S_{M}^{\ast }(\alpha ,b)\) is also considered under the same conditions. Among other things, we find convolution conditions for a function \(f\in A\) to belong to the class \(S_{M}^{\ast }(\alpha ,b)\). Several properties of the class \(S_{M}^{\ast }(n,\alpha ,b)\) are investigated.
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Claudepierre, T., C. Dalloz, D. Mornet, K. Matsumura, J. Sahel, and A. Rendon. "Characterization of the intermolecular associations of the dystrophin-associated glycoprotein complex in retinal Muller glial cells." Journal of Cell Science 113, no. 19 (October 1, 2000): 3409–17. http://dx.doi.org/10.1242/jcs.113.19.3409.
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The abnormal retinal neurotransmission observed in Duchenne muscular dystrophy patients has been attributed to altered expression of C-terminal products of the dystrophin gene in this tissue. Muller glial cells from rat retina express dystrophin protein Dp71, utrophin and the members of the dystrophin-associated glycoprotein complex (DGC), namely beta-dystroglycan, delta- and gamma-sarcoglycans and alpha1-syntrophin. The DGC could function in muscle as a link between the cystoskeleton and the extracellular matrix, as well as a signaling complex. However, other than in muscle the composition and intermolecular associations among members of the DGC are still unknown. Here we demonstrate that Dp71 and/or utrophin from rat retinal Muller glial cells form a complex with beta-dystroglycan, delta-sarcoglycan and alpha1-syntrophin. We also show that beta-dystroglycan is associated with alpha-dystrobrevin-1 and PSD-93 and that anti-PSD antibodies coimmunoprecipitated alpha-syntrophin with PSD-93. By overlay experiments we also found that Dp71and/or utrophin and alpha-dystroglycan from Muller cells could bind to actin and laminin, respectively. These results indicate that the DGC could have both structural and signaling functions in retina. On the basis of our accumulated evidence, we propose a hypothetical model for the molecular organization of the dystrophin-associated glycoprotein complex in retinal Muller glial cells, which would be helpful for understanding its function in the central nervous system.
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Wu, G., FJ Meloni, and SS Shapiro. "Platelet glycoprotein (Gp) IX associates with GpIb alpha in the platelet membrane GpIb complex." Blood 87, no. 7 (April 1, 1996): 2782–87. http://dx.doi.org/10.1182/blood.v87.7.2782.bloodjournal8772782.
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The platelet membrane glycoprotein (Gp) Ib complex consists of four polypeptides: the disulfide-linked GpIb alpha and GpIb beta subunits; GpIX, tightly, but noncovalently associated with GpIb alpha-beta; and the more weakly associated GpV. It is not certain whether the association of GpIX to Gplb alpha-beta is via GpIB alpha, GpIb beta, or both subunits, although recently published evidence implicates an interaction with GpIb beta. We have investigated the interaction of GpIX with GpIb alpha-beta using polyclonal rabbit antibodies to GpIb alpha and GpIb beta raised by immunization with purified glycocalicin and with synthetic peptide sequences from GpIb beta, respectively, as well as monoclonal antibodies directed against GpIX (FMC-25) and against GpIb alpha (AP-1). We performed two types of experiments, using either purified GpIb complex or platelets. (1) When wells were coated with nonreduced GpIb complex, the binding of FMC-25 was inhibited 73% by GpIb alpha antibody, but only 30% by the GpIb beta antibody; when wells were coated with reduced complex, FMC-25 binding was inhibited by the same two antibodies by 86% and 13%, respectively. When wells were coated with polyclonal GpIb alpha or GpIb beta antibodies and then incubated with reduced GpIb complex, only wells coated with GpIb alpha antibodies captured GpIX reactivity. When wells were coated with FMC-25 and then incubated with nonreduced GpIb complex, both the GpIb alpha and GpIb beta polyclonal antibodies reacted strongly; in contrast, only GpIb alpha reactivity was retained when wells coated with FMC-25 were incubated with reduced GpIb complex. In the reciprocal experiment, AP-1- coated wells incubated with either nonreduced or reduced GpIb complex bound radiolabeled FMC-25. (2) The ability of polyclonal GpIb alpha and GpIb beta antibodies to inhibit binding of FMC-25 to platelets was studied by ELISA and by flow cytometry. In both systems, FMC-25 binding was inhibited by the GpIb alpha antibody, but not significantly by the GpIb beta antibody. We conclude that GpIX is strongly associated with GpIb alpha in the purified platelet GpIb complex and in the platelet membrane.
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Miwa, K., and M. Yoshida. "The alpha 3 beta 3 complex, the catalytic core of F1-ATPase." Proceedings of the National Academy of Sciences 86, no. 17 (September 1989): 6484–87. http://dx.doi.org/10.1073/pnas.86.17.6484.
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The alpha 3 beta 3 complex was reconstituted from alpha and beta subunits of the thermophilic bacterium PS3 F1-ATPase (TF1) and then isolated. It is less stable at high and low temperatures than TF1, and the complex dissociates into subunits during native polyacrylamide gel electrophoresis. The alpha 3 beta 3 complex has about 20% of the ATPase activity of TF1. Its enzymic properties are similar to those of the native TF1, exhibiting similar cooperative kinetics as a function of ATP concentration, similar substrate specificity for nucleotide triphosphates, and the presence of two peaks in its temperature-activity profile. Differing from TF1, the ATPase activity of the alpha 3 beta 3 complex is insensitive to N3- inhibition, its divalent cation specificity is less stringent, and its optimum pH shifts to the alkaline side. The addition of the gamma subunit to the alpha 3 beta 3 complex leads to the formation of the alpha 3 beta 3 gamma complex, indicating that the alpha 3 beta 3 complex is an intermediate in the process of assembly of the holoenzyme from each subunit. These results definitely show that the essential structure for eliciting the ATPase activity of F1-ATPase is trimeric alpha beta pairs and that the kinetic cooperativity of the F1-ATPase is an inherent property of this trimeric structure but is not due to the presence of single-copy subunits. In this sense, the alpha 3 beta 3 complex is the catalytic core of F1-ATPase.
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Wang, S. G., K. A. Eakle, R. Levenson, and R. A. Farley. "Na+-K+-ATPase alpha-subunit containing Q905-V930 of gastric H+-K+-ATPase alpha preferentially assembles with H+-K+-ATPase beta." American Journal of Physiology-Cell Physiology 272, no. 3 (March 1, 1997): C923—C930. http://dx.doi.org/10.1152/ajpcell.1997.272.3.c923.
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Amino acids N886-A911 of the rat Na+-K+-ATPase alpha3-subunit were replaced by the corresponding region (Q905-V930) of the rat gastric H+-K+-ATPase alpha-subunit. The chimera (NGH26) was expressed in yeast with the rat Na+-K+ -ATPase beta1-subunit (rbeta1), the rat H+-K+-ATPase beta-subunit (HKbeta), the chimeric beta-subunit NHbeta1 (containing the carboxy-terminal ectodomain of HKbeta), or the chimeric beta-subunit HNbeta1 (containing the carboxy-terminal ectodomain of rbeta1). Increased resistance to trypsin digestion indicated that NGH26 preferentially assembled with HKbeta and NHbeta1 rather than with rbeta1 or HNbeta1. Ouabain binding also indicated that more functional complexes were assembled when NGH26 was expressed with HKbeta or NHbeta1. These results suggest that the sequence Q905-V930 interacts with the HKbeta-subunit on the extracellular side of the cell membrane. The NGH26 + HKbeta complex is less stable than alpha3 + HKbeta when heated and also has a lower binding affinity for ouabain [dissociation constant (Kd) = 63 nM] compared with alpha3 + rbeta1 or alpha3 + HKbeta (K(d) = 5-10 nM). In contrast, the NGH26+NHbeta1 complex is thermally as stable as alpha3 + rbeta1 complexes, and its ouabain binding affinity (K(d) = 10 nM) is the same as the wild type. These results indicate that the amino acids Q905-V930 of the rat gastric H+-K+-ATPase alpha-subunit preferentially associate with the extracellular domain of H+-K+-ATPase beta-subunit to form functional pump complexes and that the cytoplasmic and/or transmembrane region of the beta-subunit influences the stability of the alpha beta complexes.
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NAGAMATSU, Yoko, Naomi KUROYAMA, Jun-ichiro YAMAMOTO, Utako OKAMOTO, Yuko TSUDA, and Yoshio OKADA. "Enzymatic properties of .ALPHA.2-macroglobulin-elastase complex." Blood & Vessel 16, no. 1 (1985): 39–42. http://dx.doi.org/10.2491/jjsth1970.16.39.
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Id Betan, R. "Complex-energy shell model description of alpha decay." Journal of Physics: Conference Series 436 (April 17, 2013): 012061. http://dx.doi.org/10.1088/1742-6596/436/1/012061.
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Kurbatov, A., A. Drozd-Rzoska, S. J. Rzoska, M. Paluch, P. Malik, J. Zioło, and J. Jadżyn. "Universal Scaling of Alpha Relaxation in Complex Liquids." Zeitschrift für Naturforschung A 56, no. 12 (December 1, 2001): 893–94. http://dx.doi.org/10.1515/zna-2001-1217.
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Abstract A plot is given, showing the result of a scaling analysis of dielectric loss curves containing, apart from low molecular glass former data (glycerol, dibutyl phtalate), also loss curves of the following liquid crystalline materials, mostly in the iso tropic phase: 4-(2-methylbutyl)-4'cyanobiphenyl (5*CB, supercooled isotropic phase), 4-cyano-4-n-alkyl biphenyls (nematogens 5CB and 8CB, isotropic phase), 4-(4-cyano-4-butylcyclohexyl)-4'-octylbiphenyl (laterally substituted nema-togen, isotropic phase), and 4-n-alkyl-4'-isothiocyanatobiphe-nyl (5 and 10 BT, isotropic and SmE phases). The plot applies the scaling formula originally proposed for glassforming, super cooled liquids [Dendzik et al.7]. The result supports the recent suggestion that dielectric relaxation in the isotropic phase of nematogens may show some features typical for "glassy" mate rials.
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Weber, William J. "Alpha-Decay-Induced Amorphization in Complex Silicate Structures." Journal of the American Ceramic Society 76, no. 7 (July 1993): 1729–38. http://dx.doi.org/10.1111/j.1151-2916.1993.tb06641.x.
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Wang, X., M. Kiledjian, I. M. Weiss, and S. A. Liebhaber. "Detection and characterization of a 3' untranslated region ribonucleoprotein complex associated with human alpha-globin mRNA stability." Molecular and Cellular Biology 15, no. 3 (March 1995): 1769–77. http://dx.doi.org/10.1128/mcb.15.3.1769.
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The highly stable nature of globin mRNA is of central importance to erythroid cell differentiation. We have previously identified cytidine-rich (C-rich) segments in the human alpha-globin mRNA 3' untranslated region (alpha-3'UTR) which are critical in the maintenance of mRNA stability in transfected erythroid cells. In the present studies, we have detected trans-acting factors which interact with these cis elements to mediate this stabilizing function. A sequence-specific ribonucleoprotein (RNP) complex is assembled after incubation of the alpha-3'UTR with a variety of cytosolic extracts. This so-called alpha-complex is sequence specific and is not formed on the 3'UTR of either beta-globin or growth hormone mRNAs. Furthermore, base substitutions within the C-rich stretches which destabilize alpha-globin mRNA in vivo result in a parallel disruption of the alpha-complex in vitro. Competition studies with a series of homoribopolymers reveals a striking sensitivity of alpha-complex formation to poly(C), suggesting the presence of a poly(C)-binding activity within the alpha-complex. Three predominant proteins are isolated by alpha-3'UTR affinity chromatography. One of these binds directly to poly(C). This cytosolic poly(C)-binding protein is distinct from previously described nuclear poly(C)-binding heterogeneous nuclear RNPs and is necessary but not sufficient for alpha-complex formation. These data suggest that a messenger RNP complex formed by interaction of defined segments within the alpha-3'UTR with a limited number of cytosolic proteins, including a potentially novel poly(C)-binding protein, is of functional importance in establishing high-level stability of alpha-globin mRNA.
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Tsuji, A., T. Akamatsu, H. Nagamune, and Y. Matsuda. "Identification of targeting proteinase for rat α1-macroglobulin in vivo. Mast-cell tryptase is a major component of the α1-macroglobulin-proteinase complex endocytosed into rat liver lysosomes." Biochemical Journal 298, no. 1 (February 15, 1994): 79–85. http://dx.doi.org/10.1042/bj2980079.
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The alpha 1-macroglobulin-proteinase complex endocytosed into rat liver lysosomes was purified by a series of column chromatographic steps on concanavalin A-Sepharose, Sephacryl S-300, DEAE-cellulose and TSK gel DEAE-5PW columns. The complex contained no detectable alpha 2-macroglobulin. Studies on the substrate specificity indicated that the complex had tryptase-like activities towards various synthetic substrates, but no elastase, chymotrypsin, cathepsin-B and cathepsin-L activities. The proteinase activity was completely inhibited by di-isopropyl fluorophosphate, leupeptin and antipain, indicating that the proteinase bound to alpha 1-macroglobulin is a serine proteinase. Two protein bands (62 and 59 kDa) of the complex were labelled with [3H]diisopropyl fluorophosphate and both bands cross-reacted with anti-(mast-cell tryptase)antibody. These results suggest that mast-cell tryptase is a major targeting proteinase for alpha 1-macroglobulin in vivo. The main alpha-macroglobulin-proteinase complex in the adjuvant-treated rats was also the alpha 1-macroglobulin-tryptase complex, even though the plasma level of alpha 2-macroglobulin was elevated.
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Punt, J. A., J. L. Roberts, K. P. Kearse, and A. Singer. "Stoichiometry of the T cell antigen receptor (TCR) complex: each TCR/CD3 complex contains one TCR alpha, one TCR beta, and two CD3 epsilon chains." Journal of Experimental Medicine 180, no. 2 (August 1, 1994): 587–93. http://dx.doi.org/10.1084/jem.180.2.587.
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The stoichiometry of the subunits that comprise the T cell antigen receptor (TCR) complex is not completely known. In particular, it is uncertain whether TCR alpha and TCR beta proteins are present in the TCR complex as one or multiple heterodimeric pairs. In this study we have used mice transgenic for two different TCR alpha and two different TCR beta proteins to determine the number of TCR alpha and TCR beta chains in a single TCR complex. Individual thymocytes and splenic T cells from double TCR transgenic mice simultaneously expressed all four transgenic TCR proteins on their surfaces. Because the individual TCR alpha and individual TCR beta proteins were biochemically distinguishable, we were able to examine association among the transgenic TCR products. We found that each TCR alpha chain paired with each TCR beta chain, but that each TCR complex contained only one TCR alpha and one TCR beta protein. Furthermore, quantitative immunofluorescence revealed that T cells expressed twice as many CD3 epsilon as TCR beta proteins. These findings demonstrate that there are precisely one TCR alpha, one TCR beta, and two CD3 epsilon chains in each TCR/CD3 complex expressed on the surfaces of both thymocytes and mature T cells.
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Davis, Donald M. "SOME NEW IMMERSION RESULTS FOR COMPLEX PROJECTIVE SPACE." Proceedings of the Edinburgh Mathematical Society 51, no. 1 (February 2008): 45–56. http://dx.doi.org/10.1017/s0013091506000277.
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AbstractWe prove the following two new optimal immersion results for complex projective space. First, if $n\equiv3\,\Mod 8$ but $n\not\equiv3\,\Mod 64$, and $\alpha(n)=7$, then $CP^{n}$ can be immersed in $\mathbb{R}^{4n-14}$. Second, if $n$ is even and $\alpha(n)=3$, then $CP^n$ can be immersed in $\mathbb{R}^{4n-4}$. Here $\alpha(n)$ denotes the number of 1s in the binary expansion of $n$. The first contradicts a result of Crabb, which said that such an immersion does not exist, apparently due to an arithmetical mistake. We combine Crabb's method with that developed by the author and Mahowald.
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Geisler, C., J. Schøller, M. A. Wahi, B. Rubin, and A. Weiss. "Association of the human CD3-zeta chain with the alpha beta-T cell receptor/CD3 complex. Clues from a T cell variant with a mutated T cell receptor-alpha chain." Journal of Immunology 145, no. 6 (September 15, 1990): 1761–67. http://dx.doi.org/10.4049/jimmunol.145.6.1761.
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Abstract The TCR for Ag, on the majority of human T cells, is a disulfide-linked heterodimer composed of TCR-alpha and -beta chains noncovalently associated with the monomorphic CD3 complex composed of the CD3-gamma, -delta, -epsilon, and -zeta chains. The interactions involved in the assembly of the various components of this multimeric protein complex are not fully understood. In this report, a variant of the human leukemic T cell line Jurkat that synthesized all of the known components of the TCR/CD3 complex but fails to express the TCR/CD3 complex at the cell surface is further characterized. This variant, J79, has a mutated TCR-alpha chain that does not affect the assembly of the pentameric form (TCR-alpha beta-CD3-gamma delta epsilon) of the TCR/CD3 complex but inhibits the assembly of the CD3-zeta homodimer with the rest of the complex (TCR-alpha beta-CD3-gamma delta epsilon----TCR-alpha beta-CD3-gamma delta epsilon zeta 2). Transfecting a wild-type TCR-alpha gene into J79 reconstituted expression of a complete functionally competent TCR/CD3 complex at the cell surface. The results indicate that the TCR-alpha chain plays a crucial role in the assembly of the CD3-zeta homodimer with the pentameric form of the TCR/CD3 complex.
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Hall, R. K., D. K. Scott, E. L. Noisin, P. C. Lucas, and D. K. Granner. "Activation of the phosphoenolpyruvate carboxykinase gene retinoic acid response element is dependent on a retinoic acid receptor/coregulator complex." Molecular and Cellular Biology 12, no. 12 (December 1992): 5527–35. http://dx.doi.org/10.1128/mcb.12.12.5527-5535.1992.
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The accessory factor 1 (AF1) element is an upstream transcriptional control region that plays a role in the response of the phosphoenolpyruvate carboxykinase (PEPCK) gene to both glucocorticoids and retinoic acid. We demonstrate here that retinoic acid receptor alpha (RAR alpha) binds to a sequence within the AF1 element, TGACCT (site B), that is a consensus retinoic acid response element (RARE) half-site. A similar DNA sequence, TGGCCG (site C), located 1 bp downstream of site B, is not involved in the binding of RAR alpha monomers or dimers but is required for the constitution of a functional RARE. Site C is also required for the formation of a complex involving RAR alpha and a liver nuclear factor designated CR, for coregulator. Mutational analysis of the AF1 element shows that the RAR alpha/CR complex is the trans-acting unit that mediates the retinoic acid response of the PEPCK gene. Another member of the retinoid receptor family, retinoid X receptor alpha (RXR alpha), can also form a complex with RAR alpha and the AF1 element. Several observations, including the observation that RXR alpha antibody interacts with CR, indicate that RXR alpha and CR are identical or closely related proteins. Through RXR alpha forms a complex with RAR alpha and the AF1 element, we demonstrate that the AF1 element is functionally distinguishable from a retinoid X response element. Taken together, our results show that the AF1 element contains an RARE that mediates a retinoic acid response by binding an RAR alpha/coregulator complex; this coregulator is presumably RXR alpha.
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Hall, R. K., D. K. Scott, E. L. Noisin, P. C. Lucas, and D. K. Granner. "Activation of the phosphoenolpyruvate carboxykinase gene retinoic acid response element is dependent on a retinoic acid receptor/coregulator complex." Molecular and Cellular Biology 12, no. 12 (December 1992): 5527–35. http://dx.doi.org/10.1128/mcb.12.12.5527.
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The accessory factor 1 (AF1) element is an upstream transcriptional control region that plays a role in the response of the phosphoenolpyruvate carboxykinase (PEPCK) gene to both glucocorticoids and retinoic acid. We demonstrate here that retinoic acid receptor alpha (RAR alpha) binds to a sequence within the AF1 element, TGACCT (site B), that is a consensus retinoic acid response element (RARE) half-site. A similar DNA sequence, TGGCCG (site C), located 1 bp downstream of site B, is not involved in the binding of RAR alpha monomers or dimers but is required for the constitution of a functional RARE. Site C is also required for the formation of a complex involving RAR alpha and a liver nuclear factor designated CR, for coregulator. Mutational analysis of the AF1 element shows that the RAR alpha/CR complex is the trans-acting unit that mediates the retinoic acid response of the PEPCK gene. Another member of the retinoid receptor family, retinoid X receptor alpha (RXR alpha), can also form a complex with RAR alpha and the AF1 element. Several observations, including the observation that RXR alpha antibody interacts with CR, indicate that RXR alpha and CR are identical or closely related proteins. Through RXR alpha forms a complex with RAR alpha and the AF1 element, we demonstrate that the AF1 element is functionally distinguishable from a retinoid X response element. Taken together, our results show that the AF1 element contains an RARE that mediates a retinoic acid response by binding an RAR alpha/coregulator complex; this coregulator is presumably RXR alpha.
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Kiledjian, M., C. T. DeMaria, G. Brewer, and K. Novick. "Identification of AUF1 (heterogeneous nuclear ribonucleoprotein D) as a component of the alpha-globin mRNA stability complex." Molecular and Cellular Biology 17, no. 8 (August 1997): 4870–76. http://dx.doi.org/10.1128/mcb.17.8.4870.
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mRNA turnover is an important regulatory component of gene expression and is significantly influenced by ribonucleoprotein (RNP) complexes which form on the mRNA. Studies of human alpha-globin mRNA stability have identified a specific RNP complex (alpha-complex) which forms on the 3' untranslated region (3'UTR) of the mRNA and appears to regulate the erythrocyte-specific accumulation of alpha-globin mRNA. One of the protein activities in this multiprotein complex is a poly(C)-binding activity which consists of two proteins, alphaCP1 and alphaCP2. Neither of these proteins, individually or as a pair, can bind the alpha-globin 3'UTR unless they are complexed with the remaining non-poly(C) binding proteins of the alpha-complex. With the yeast two-hybrid screen, a second alpha-complex protein was identified. This protein is a member of the previously identified A+U-rich (ARE) binding/degradation factor (AUF1) family of proteins, which are also known as the heterogeneous nuclear RNP (hnRNP) D proteins. We refer to these proteins as AUF1/hnRNP-D. Thus, a protein implicated in ARE-mediated mRNA decay is also an integral component of the mRNA stabilizing alpha-complex. The interaction of AUF1/hnRNP-D is more efficient with alphaCP1 relative to alphaCP2 both in vitro and in vivo, suggesting that the alpha-complex might be dynamic rather than a fixed complex. AUF1/hnRNP-D could, therefore, be a general mRNA turnover factor involved in both stabilization and decay of mRNA.
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Hynes, R. O., E. E. Marcantonio, M. A. Stepp, L. A. Urry, and G. H. Yee. "Integrin heterodimer and receptor complexity in avian and mammalian cells." Journal of Cell Biology 109, no. 1 (July 1, 1989): 409–20. http://dx.doi.org/10.1083/jcb.109.1.409.
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We report data showing that the integrin receptor complex in chickens contains several discrete heterodimers all sharing the beta 1-integrin subunit combined separately with different alpha-subunits. Using antisera to synthetic peptides based on cDNA sequences of chicken and human alpha-integrin subunits to analyze the integrin complement of avian and mammalian cells, we show that band 2 of the chicken integrin complex contains alpha-subunits related to both alpha 3- and alpha 5-subunits of human integrins. alpha 3 beta 1 and alpha 5 beta 1 have both previously been shown in human cells to be fibronectin receptors and alpha 3 beta 1 can also act as a receptor for laminin and collagen. We also provide evidence for the presence, in band 1 of the chicken integrin complex, of a third integrin alpha-subunit which is also alpha 5 related. This integrin subunit exists in a separate heterodimer complex with beta 1 and binds to fibronectin-affinity columns. These results provide explanations for published data showing that the avian integrin complex contains receptor activity for a variety of extracellular matrix proteins. We conclude that the chicken integrin complex comprises a set of beta 1-integrin heterodimers equivalent to the human VLA antigens and includes at least two fibronectin receptors. Finally, we show that chicken embryo fibroblasts also contain a beta 3-class integrin related to the RGD receptors defined in various human cells.
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Caston, Emily. "Dossier: Screen Advertising. Introduction." Alphaville: journal of film and screen media, no. 25 (August 30, 2023): 61–68. http://dx.doi.org/10.33178/alpha.25.04.
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The purpose of this dossier is to ask, “What is screen advertising and what relevance, if any, does it have for film and television studies?” Both are large and complex questions, but the second is perhaps the bolder and, therefore, a question that will remain unanswered. It invokes a larger conversation about the nature of film studies in the academy since it emerged within the paradigm of literary studies in Britain and the USA in the 1970s. To answer these questions, the dossier presents interviews with three influential figures from screen advertising production, two reports about advertising archives and an article about the industry in Britain since 1955.
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Mimuro, J., Y. Koike, Y. Sumi, and N. Aoki. "Monoclonal antibodies to discrete regions in alpha 2-plasmin inhibitor." Blood 69, no. 2 (February 1, 1987): 446–53. http://dx.doi.org/10.1182/blood.v69.2.446.446.
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Abstract Three monoclonal antibodies to alpha 2-plasmin inhibitor (alpha 2PI) were characterized. The first, JTPI-1, was directed against the reative site of alpha 2PI and inhibited antiplasmin activity by interfering with the formation of alpha 2PI-plasmin complexes. The avidity of JTPI- 1 to the preformed alpha 2PI-plasmin complex was markedly lower than that to free alpha 2PI, which made this antibody useful for measuring the free alpha 2PI in plasma. The second, JTPI-2, recognized an epitope in the C-terminal fragment of alpha 2PI (11,000 daltons [11 K]) that was cleaved from alpha 2PI by plasmin upon complex formation but remained noncovalently attached to the complex. However, binding of JTPI-2 to alpha 2PI was not inhibited by the C-terminal 26-residue peptide containing the plasminogen-binding site and had no effect on the function of alpha 2PI. These data suggested that JTPI-2 recognized an epitope between the C-terminal 26-residue peptide and the reactive site. The third, JTPI-3, bound the alpha 2PI-plasmin complex (150 K) as well as alpha 2PI. Binding was inhibited by the N-terminal 12-residue peptide of alpha 2PI, but factor XIII-catalyzed cross-linking of alpha 2PI to fibrin was not inhibited by JTPI-3. These results suggested that the antibody recognized an epitope near the N terminus. These three monoclonal antibodies were useful for analyzing the mechanism of interaction between alpha 2PI and plasmin.
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Mimuro, J., Y. Koike, Y. Sumi, and N. Aoki. "Monoclonal antibodies to discrete regions in alpha 2-plasmin inhibitor." Blood 69, no. 2 (February 1, 1987): 446–53. http://dx.doi.org/10.1182/blood.v69.2.446.bloodjournal692446.
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Three monoclonal antibodies to alpha 2-plasmin inhibitor (alpha 2PI) were characterized. The first, JTPI-1, was directed against the reative site of alpha 2PI and inhibited antiplasmin activity by interfering with the formation of alpha 2PI-plasmin complexes. The avidity of JTPI- 1 to the preformed alpha 2PI-plasmin complex was markedly lower than that to free alpha 2PI, which made this antibody useful for measuring the free alpha 2PI in plasma. The second, JTPI-2, recognized an epitope in the C-terminal fragment of alpha 2PI (11,000 daltons [11 K]) that was cleaved from alpha 2PI by plasmin upon complex formation but remained noncovalently attached to the complex. However, binding of JTPI-2 to alpha 2PI was not inhibited by the C-terminal 26-residue peptide containing the plasminogen-binding site and had no effect on the function of alpha 2PI. These data suggested that JTPI-2 recognized an epitope between the C-terminal 26-residue peptide and the reactive site. The third, JTPI-3, bound the alpha 2PI-plasmin complex (150 K) as well as alpha 2PI. Binding was inhibited by the N-terminal 12-residue peptide of alpha 2PI, but factor XIII-catalyzed cross-linking of alpha 2PI to fibrin was not inhibited by JTPI-3. These results suggested that the antibody recognized an epitope near the N terminus. These three monoclonal antibodies were useful for analyzing the mechanism of interaction between alpha 2PI and plasmin.
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Shum, L., S. A. Reeves, A. C. Kuo, E. S. Fromer, and R. Derynck. "Association of the transmembrane TGF-alpha precursor with a protein kinase complex." Journal of Cell Biology 125, no. 4 (May 15, 1994): 903–16. http://dx.doi.org/10.1083/jcb.125.4.903.
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A variety of growth factors including transforming growth factor-alpha (TGF-alpha) are synthesized as transmembrane precursors. The short cytoplasmic domain of the transmembrane TGF-alpha precursor lacks any apparent motif associated with signal transduction. However, the sequence conservation of this cytoplasmic domain and its abundance of cysteine residues, reminiscent of the cytoplasmic domains of CD4 and CD8, suggest a biological function. In this study, we showed that transmembrane TGF-alpha was rapidly internalized after interaction with a specific antibody and that this internalization was greatly decreased when the COOH-terminal 31 amino acids were removed. Chemical cross-linking experiments revealed two associated proteins of 86 and 106 kD which coimmunoprecipitated with the TGF-alpha precursor. The association of p86 was dependent on the presence of the COOH-terminal cytoplasmic 31 amino acids of the TGF-alpha precursor, whereas p106 still remained associated when this segment was deleted. In addition, p106 was tyrosine-phosphorylated and exposed on the cell surface. The protein complex associated with transmembrane TGF-alpha displayed kinase activities towards tyrosine, serine, and threonine residues. These activities were not associated with transmembrane TGF-alpha when the COOH-terminal segment was truncated. The association of a protein kinase complex with transmembrane TGF-alpha may provide the basic elements for a "reverse" mode of signaling through the cytoplasmic domain of this growth factor, which may lead to two-directional communication during ligand-receptor interaction.
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Hinck, L., I. S. Näthke, J. Papkoff, and W. J. Nelson. "Dynamics of cadherin/catenin complex formation: novel protein interactions and pathways of complex assembly." Journal of Cell Biology 125, no. 6 (June 15, 1994): 1327–40. http://dx.doi.org/10.1083/jcb.125.6.1327.
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Calcium-dependent cell-cell adhesion is mediated by the cadherin family of cell adhesion proteins. Transduction of cadherin adhesion into cellular reorganization is regulated by cytosolic proteins, termed alpha-, beta-, and gamma-catenin (plakoglobin), that bind to the cytoplasmic domain of cadherins and link them to the cytoskeleton. Previous studies of cadherin/catenin complex assembly and organization relied on the coimmunoprecipitation of the complex with cadherin antibodies, and were limited to the analysis of the Triton X-100 (TX-100)-soluble fraction of these proteins. These studies concluded that only one complex exists which contains cadherin and all of the catenins. We raised antibodies specific for each catenin to analyze each protein independent of its association with E-cadherin. Extracts of Madin-Darby canine kidney epithelial cells were sequentially immunoprecipitated and immunoblotted with each antibody, and the results showed that there were complexes of E-cadherin/alpha-catenin, and either beta-catenin or plakoglobin in the TX-100-soluble fraction. We analyzed the assembly of cadherin/catenin complexes in the TX-100-soluble fraction by [35S]methionine pulse-chase labeling, followed by sucrose density gradient fractionation of proteins. Immediately after synthesis, E-cadherin, beta-catenin, and plakoglobin cosedimented as complexes. alpha-Catenin was not associated with these complexes after synthesis, but a subpopulation of alpha-catenin joined the complex at a time coincident with the arrival of E-cadherin at the plasma membrane. The arrival of E-cadherin at the plasma membrane coincided with an increase in its insolubility in TX-100, but extraction of this insoluble pool with 1% SDS disrupted the cadherin/catenin complex. Therefore, to examine protein complex assembly in both the TX-100-soluble and -insoluble fractions, we used [35S]methionine labeling followed by chemical cross-linking before cell extraction. Analysis of cross-linked complexes from cells labeled to steady state indicates that, in addition to cadherin/catenin complexes, there were cadherin-independent pools of catenins present in both the TX-100-soluble and -insoluble fractions. Metabolic labeling followed by chase showed that immediately after synthesis, cadherin/beta-catenin, and cadherin/plakoglobin complexes were present in the TX-100-soluble fraction. Approximately 50% of complexes were titrated into the TX-100-insoluble fraction coincident with the arrival of the complexes at the plasma membrane and the assembly of alpha-catenin. Subsequently, > 90% of labeled cadherin, but no additional labeled catenin complexes, entered the TX-100-insoluble fraction.(ABSTRACT TRUNCATED AT 400 WORDS)
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Handyside, Fiona. "Girlhood, postfeminism and contemporary female art-house authorship." Alphaville: Journal of Film and Screen Media, no. 10 (December 16, 2015): 31–48. http://dx.doi.org/10.33178/alpha.10.02.
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Both Sofia Coppola and Mia Hansen-Løve’s first three films can be understood as trilogies of female coming of age. These are thematic or conceptual trilogies, declared as such after the fact by their directors, and thus a self-conscious declaration of authorial agency, but the trilogy itself is not given a definitive name. This article explores the complex position these trilogies thus occupy. On the one hand, they testify to the impact of feminist activism and theorising on filmmaking, as they demonstrate the creative power and autonomy of the postfeminist auteur. On the other, they concentrate on narrow, girlish worlds, and remain marked by hesitancy and containment, demonstrating the persistent restrictions for women within postfeminist cultural norms.
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Geisler, C., J. Kuhlmann, and B. Rubin. "Assembly, intracellular processing, and expression at the cell surface of the human alpha beta T cell receptor/CD3 complex. Function of the CD3-zeta chain." Journal of Immunology 143, no. 12 (December 15, 1989): 4069–77. http://dx.doi.org/10.4049/jimmunol.143.12.4069.
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Abstract The TCR/CD3 complex is a multimeric protein complex composed of a minimum of seven transmembrane chains (TCR alpha beta-CD3 gamma delta epsilon zeta 2). Whereas earlier studies have demonstrated that both the TCR-alpha and -beta chains are required for the cell surface expression of the TCR/CD3 complex, the role of the CD3 chains for the TCR/CD3 expression have not been experimentally addressed in human T cells. In this study the function of the CD3-zeta chain for the assembly, intracellular processing, and expression of the TCR/CD3 complex in the human leukemic T cell line Jurkat was investigated. The results indicate that: 1) CD3-zeta is required for the cell surface expression of the TCR/CD3 complex; 2) the pentameric form (TCR alpha beta-CD3 gamma delta epsilon) of the TCR/CD3 complex and single TCR chains associated with CD3 (TCR alpha-CD3 gamma delta epsilon and TCR beta-CD3 gamma delta epsilon) are produced in the endoplasmic reticulum in the absence of CD3-zeta; 3) the CD3-zeta does not associate with TCR alpha-CD3 gamma delta epsilon or TCR beta-CD3 gamma delta epsilon complexes; 4) CD3-zeta associate with the pentameric form of the TCR/CD3 complex in the endoplasmic reticulum to form the heptameric complex (TCR alpha beta-CD3 gamma delta epsilon----TCR alpha beta-CD3 gamma delta epsilon 2); and 5) CD3-zeta is required for the export of the TCR/CD3 complex from the endoplasmic reticulum to the Golgi apparatus for subsequent processing.
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Darus, Maslina, and Imran Faisal. "Some subclasses of analytic functions of complex order defined by new differential operator." Tamkang Journal of Mathematics 43, no. 2 (June 30, 2012): 223–42. http://dx.doi.org/10.5556/j.tkjm.43.2012.740.
Full textAbstract:
Let \hskip 2pt $\mathcal{A}(n)$ \hskip 2pt denote \hskip 2pt the \hskip 2pt class \hskip 2pt of \hskip 2pt analytic \hskip 2pt functions \hskip 2pt $f$ \hskip 2pt in \hskip 2pt the \hskip 2pt open \hskip 2pt unit \hskip 2pt disk \hskip 2pt $U=\{z:|z|<1\}$ \hskip 2pt normalized \hskip 2pt by \hskip 2pt $f(0)=f'(0)-1=0.$ \hskip 2pt In \hskip 2pt this \hskip 2pt paper, \hskip 2pt we \hskip 2pt introduce \hskip 2pt and \hskip 2pt study \hskip 2pt the \hskip 2pt classes \hskip 2pt $S_{n, \mu}(\gamma, \alpha, \beta, \lambda, \mho)$ \hskip 2pt and \hskip 2pt $R_{n, \mu}(\gamma, \alpha, \beta, \lambda, \mho)$ \hskip 2pt of \hskip 2pt functions \hskip 2pt $f\in\mathcal{A}(n)$ with $(\mu)z(D^{\mho+2}_{\lambda}(\alpha, \omega)f(z))'+(1-\mu)z(D^{\mho+1}_{\lambda}(\alpha, \omega)f(z))'\neq0$ and satisfy some conditions available in literature, where $f\in\mathcal{A}(n), \alpha, \omega, \lambda, \mu \geq0, \mho\in \mathbb{N}\cup\{0\},\,\,z\in U,$ and $D^{m}_{\lambda}(\alpha, \omega)f(z): \mathcal{A}\rightarrow \mathcal{A},$ is the linear fractional differential operator, newly defined as follows $$D^{m}_{\lambda}(\alpha, \omega)f(z) = z+ \sum\limits_{k=2}^{\infty}a_{k}(1+(k-1)\lambda \omega^{\alpha})^{m}z^{k}\cdot$$ Several properties such as coefficient estimates, growth and distortion theorems, extreme points, integral means inequalities and inclusion for the functions included in the classes $S_{n, \mu}(\gamma, \alpha, \beta, \lambda, \mho, \omega)$ and $R_{n, \mu}(\gamma, \alpha, \beta, \lambda, \mho, \omega)$ are given.
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Worley, D. S., J. M. Pisano, E. D. Choi, L. Walus, C. A. Hession, R. L. Cate, M. Sanicola, and S. J. Birren. "Developmental regulation of GDNF response and receptor expression in the enteric nervous system." Development 127, no. 20 (October 15, 2000): 4383–93. http://dx.doi.org/10.1242/dev.127.20.4383.
Full textAbstract:
The development of the enteric nervous system is dependent upon the actions of glial cell line-derived neurotrophic factor (GDNF) on neural crest-derived precursor cells in the embryonic gut. GDNF treatment of cultured enteric precursor cells leads to an increase in the number of neurons that develop and/or survive. Here we demonstrate that, although GDNF promoted an increase in neuron number at all embryonic ages examined, there was a developmental shift from a mitogenic to a trophic response by the developing enteric neurons. The timing of this shift corresponded to developmental changes in gut expression of GFR alpha-1, a co-receptor in the GDNF-Ret signaling complex. GFR alpha-1 was broadly expressed in the gut at early developmental stages, at which times soluble GFR alpha-1 was released into the medium by cultured gut cells. At later times, GFR alpha-1 became restricted to neural crest-derived cells. GFR alpha-1 could participate in GDNF signaling when expressed in cis on the surface of enteric precursor cells, or as a soluble protein. The GDNF-mediated response was greater when cell surface, compared with soluble, GFR alpha-1 was present, with the maximal response seen the presence of both cis and trans forms of GFR alpha-1. In addition to contributing to GDNF signaling, cell-surface GFR alpha-1 modulated the specificity of interactions between GDNF and soluble GFR alphas. These experiments demonstrate that complex, developmentally regulated, signaling interactions contribute to the GDNF-dependent development of enteric neurons.
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Peterson, C. G., and P. Venge. "Interaction and complex-formation between the eosinophil cationic protein and α2-macroglobulin." Biochemical Journal 245, no. 3 (August 1, 1987): 781–87. http://dx.doi.org/10.1042/bj2450781.
Full textAbstract:
The interaction between the highly basic and cytotoxic eosinophil cationic protein (ECP) and human plasma proteins is described. The major plasma protein responsible for complex-formation with ECP was shown to be the ‘fast’ form of alpha 2-macroglobulin (alpha 2M). Large amounts of complexes were observed in a serum obtained from a patient with hypereosinophilic syndrome. The amount of complexes that could be generated in vitro in normal fresh serum was rather low and was even less in fresh citrated plasma. Complex-formation between the non-proteolytic ECP and alpha 2M was augmented in the presence of methylamine. Binding of ECP to alpha 2M was also induced by the proteinases cathepsin G and thrombin, and the binding was competitive with cathepsin G. Methylamine and the proteinases seem to share a common mechanism in inducing binding of ECP. The nature of the ECP-alpha 2M interaction is non-covalent, but withstands high salt concentrations. The interaction with alpha 2M may reflect a mechanism by which the organism protects itself against the deleterious effects of the highly cytotoxic protein ECP.
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Ozawa, M., and R. Kemler. "Molecular organization of the uvomorulin-catenin complex." Journal of Cell Biology 116, no. 4 (February 15, 1992): 989–96. http://dx.doi.org/10.1083/jcb.116.4.989.
Full textAbstract:
The Ca(2+)-dependent cell adhesion molecule uvomorulin is a member of the cadherin gene family. Its cytoplasmic region complexes with structurally defined proteins termed alpha-, beta-, and gamma-catenins. Here we show that A-CAM (N-cadherin), another member of this gene family, also associates with catenins suggesting that this complex formation may be a general property of the cadherins. For uvomorulin it has been found that this association with catenins is of crucial importance for the adhesive function, but little is known about the molecular organization of the uvomorulin-catenin complex. Using a combination of biochemical analyses we show that a single complex is composed of one molecule of uvomorulin, one or two molecules of beta-catenin, and one molecule of alpha-catenin. Furthermore, beta-catenin seems to interact more directly with uvomorulin. In pulse-chase experiments beta-catenin is already associated with the 135-kD uvomorulin precursor molecule but the assembly of the newly synthesized alpha-catenin into the complex is only detected around the time of endoproteolytic processing.
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Treadway, J. L., B. D. Morrison, J. A. Wemmie, I. Frias, T. O'Hare, P. F. Pilch, and J. E. Pessin. "The endogenous functional turkey erythrocyte and rat liver insulin receptor is an α2β2 heterotetrameric complex." Biochemical Journal 271, no. 1 (October 1, 1990): 99–105. http://dx.doi.org/10.1042/bj2710099.
Full textAbstract:
Previous studies have indicated that turkey erythrocyte and rat liver membranes contain endogenous alpha beta heterodimeric insulin receptors in addition to the disulphide-linked alpha 2 beta 2 heterotetrameric complexes characteristic of most cell types. We utilized 125I-insulin affinity cross-linking to examine the structural properties of insulin receptors from rat liver and turkey erythrocyte membranes prepared in the absence and presence of sulphydryl alkylating agents. Rat liver membranes prepared in the absence of sulphydryl alkylating agents displayed specific labelling of Mr 400,000 and 200,000 bands, corresponding to the alpha 2 beta 2 heterotetrameric and alpha beta heterodimeric insulin receptor complexes respectively. In contrast, affinity cross-linking of membranes prepared with iodoacetamide (IAN) or N-ethylmaleimide identified predominantly the alpha 2 beta 2 heterotetrameric insulin receptor complex. Similarly, affinity cross-linking and solubilization of intact turkey erythrocytes in the presence of IAN resulted in exclusive labelling of the alpha 2 beta 2 heterotetrameric insulin receptor complex, whereas in the absence of IAN both alpha 2 beta 2 and alpha beta species were observed. Turkey erythrocyte alpha 2 beta 2 heterotetrameric insulin receptors from IAN-protected membranes displayed a 3-4-fold stimulation of beta subunit autophosphorylation and substrate phosphorylation by insulin, equivalent to that observed in intact human placenta insulin receptors. Turkey erythrocyte alpha beta heterodimeric insulin receptors, prepared by defined pH/dithiothreitol treatment of IAN-protected membranes, were also fully competent in insulin-stimulated protein kinase activity compared with alpha beta heterodimeric human placenta receptors. In contrast, endogenous turkey erythrocyte alpha beta heterodimeric insulin receptors displayed basal protein kinase activity which was insulin-insensitive. These data indicate that native turkey erythrocyte and rat liver insulin receptors are structurally and functionally similar to alpha 2 beta 2 heterotetrameric human placenta insulin receptors. The alpha beta heterodimeric insulin receptors previously identified in these tissues most likely resulted from disulphide bond reduction and denaturation of the alpha 2 beta 2 holoreceptor complexes during membrane preparation.