Relevant bibliographies by topics / HAP1

Academic literature on the topic 'HAP1'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'HAP1.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "HAP1"

1

Rong, Juan, Shihua Li, Guoqing Sheng, Meng Wu, Brian Coblitz, Min Li, Haian Fu, and Xiao-Jiang Li. "14-3-3 Protein Interacts with Huntingtin-associated Protein 1 and Regulates Its Trafficking." Journal of Biological Chemistry 282, no. 7 (December 13, 2006): 4748–56. http://dx.doi.org/10.1074/jbc.m609057200.

Full text
Abstract:
HAP1 (Huntingtin-associated protein 1) consists of two alternately spliced isoforms (HAP1A and HAP1B, which have unique C-terminal sequences) and participates in intracellular trafficking. The C terminus of HAP1A is phosphorylated, and this phosphorylation was found to decrease the association of HAP1A with kinesin light chain, a protein involved in anterograde transport in cells. It remains unclear how this phosphorylation functions to regulate the association of HAP1 with trafficking proteins. Using the yeast two-hybrid system, we found that HAP1 also interacts with 14-3-3 proteins, which are involved in the assembly of protein complexes and the regulation of protein trafficking. The interaction of HAP1 with 14-3-3 is confirmed by their immunoprecipitation and colocalization in mouse brain. Moreover, this interaction is specific to HAP1A and is increased by the phosphorylation of the C terminus of HAP1A. We also found that expression of 14-3-3 decreases the association of HAP1A with kinesin light chain. As a result, there is less HAP1A distributed in neurite tips of PC12 cells that overexpress 14-3-3. Also, overexpression of 14-3-3 reduces the effect of HAP1A in promoting neurite outgrowth of PC12 cells. We propose that the phosphorylation-dependent interaction of HAP1A with 14-3-3 regulates HAP1 function by influencing its association with kinesin light chain and trafficking in neuronal processes.
APA, Harvard, Vancouver, ISO, and other styles
2

Schneider, J. C., and L. Guarente. "Regulation of the yeast CYT1 gene encoding cytochrome c1 by HAP1 and HAP2/3/4." Molecular and Cellular Biology 11, no. 10 (October 1991): 4934–42. http://dx.doi.org/10.1128/mcb.11.10.4934.

Full text
Abstract:
Mitochondrial biogenesis requires the coordinate induction of hundreds of genes that reside in the nucleus. We describe here a study of the regulation of the nuclear-encoded cytochrome c1 of the b-c1 complex. Unlike cytochrome c, which is encoded by two genes, CYC1 and CYC7, c1 is encoded by a single gene, CYT1. The regulatory region of the CYT1 promoter contains binding sites for the HAP1 and HAP2/3/4 transactivators that regulate CYC1. The binding of HAP1 to the CYT1 element was studied in detail and found to differ in two important respects from binding to the CYC1 element. First, while CYC1 contains two sites that bind HAP1 cooperatively, CYT1 has a single high-affinity site. Second, while the CYT1 site and the stronger HAP1-binding site of CYC1 share a large block of homology, the HAP1 footprints at these sites are offset by several nucleotides. We discuss how these differences in HAP1 binding might relate to the difference in the biology of cytochrome c and cytochrome c1.
APA, Harvard, Vancouver, ISO, and other styles
3

Schneider, J. C., and L. Guarente. "Regulation of the yeast CYT1 gene encoding cytochrome c1 by HAP1 and HAP2/3/4." Molecular and Cellular Biology 11, no. 10 (October 1991): 4934–42. http://dx.doi.org/10.1128/mcb.11.10.4934-4942.1991.

Full text
Abstract:
Mitochondrial biogenesis requires the coordinate induction of hundreds of genes that reside in the nucleus. We describe here a study of the regulation of the nuclear-encoded cytochrome c1 of the b-c1 complex. Unlike cytochrome c, which is encoded by two genes, CYC1 and CYC7, c1 is encoded by a single gene, CYT1. The regulatory region of the CYT1 promoter contains binding sites for the HAP1 and HAP2/3/4 transactivators that regulate CYC1. The binding of HAP1 to the CYT1 element was studied in detail and found to differ in two important respects from binding to the CYC1 element. First, while CYC1 contains two sites that bind HAP1 cooperatively, CYT1 has a single high-affinity site. Second, while the CYT1 site and the stronger HAP1-binding site of CYC1 share a large block of homology, the HAP1 footprints at these sites are offset by several nucleotides. We discuss how these differences in HAP1 binding might relate to the difference in the biology of cytochrome c and cytochrome c1.
APA, Harvard, Vancouver, ISO, and other styles
4

Yang, Miao, Yoon Lim, Xiaojiang Li, Jin-Hua Zhong, and Xin-Fu Zhou. "Precursor of Brain-derived Neurotrophic Factor (proBDNF) Forms a Complex with Huntingtin-associated Protein-1 (HAP1) and Sortilin That Modulates proBDNF Trafficking, Degradation, and Processing." Journal of Biological Chemistry 286, no. 18 (February 28, 2011): 16272–84. http://dx.doi.org/10.1074/jbc.m110.195347.

Full text
Abstract:
proBDNF, a precursor of brain-derived neurotrophic factor (BDNF), is anterogradely transported and released from nerve terminals, but the mechanism underlying this process remains unclear. In this study, we report that proBDNF forms a complex with Huntingtin associated protein-1 (HAP1) and sortilin, which plays an important role in proBDNF intracellular trafficking and stabilization. The interaction of proBDNF with both HAP1A and sortilin in co-transfected HEK293 cells is confirmed by both fluorescence resonance energy transfer and co-immunoprecipitation. The frequent co-localization (>90%) of endogenous HAP1, sortilin, and proBDNF is also found in cultured cortical neurons. Mapping studies using GST pulldown and competition assays has defined the interacting region of HAP1 with proBDNF within amino acids 371–445 and the binding sequences of proBDNF to HAP1 between amino acids 65 and 90. Fluorescence recovery after photobleaching confirms the defective movement of proBDNF-containing vesicles in neurites of HAP1−/− neurons, which can be partially restored by reintroducing HAP1 cDNA into the neurons. However, the effect is significantly increased by simultaneously reintroducing both HAP1 and sortilin. proBDNF and HAP1 are highly co-localized with organelle markers for the Golgi network, microtubules, molecular motor, or endosomes in normal neurons, but this co-localization is reduced in HAP1−/− neurons. Co-immunoprecipitation and Western blot showed that sortilin stabilizes the proBDNF·HAP1 complex in co-transfected HEK293 cells, helping to prevent proBDNF degradation. Furthermore, the complex facilitates furin cleavage to release mature BDNF.
APA, Harvard, Vancouver, ISO, and other styles
5

Lee, Hee Chul, Thomas Hon, Changgui Lan, and Li Zhang. "Structural Environment Dictates the Biological Significance of Heme-Responsive Motifs and the Role of Hsp90 in the Activation of the Heme Activator Protein Hap1." Molecular and Cellular Biology 23, no. 16 (August 15, 2003): 5857–66. http://dx.doi.org/10.1128/mcb.23.16.5857-5866.2003.

Full text
Abstract:
ABSTRACT Heme-responsive motifs (HRMs) mediate heme regulation of diverse regulatory proteins. The heme activator protein Hap1 contains seven HRMs, but only one of them, HRM7, is essential for heme activation of Hap1. To better understand the molecular basis underlying the biological significance of HRMs, we examined the effects of various mutations of HRM7 on Hap1. We found that diverse mutations of HRM7 significantly diminished the extent of Hap1 activation by heme and moderately enhanced the interaction of Hap1 with Hsp90. Furthermore, deletions of nonregulatory sequences completely abolished heme activation of Hap1 and greatly enhanced the interaction of Hap1 with Hsp90. These results show that the biological functions of HRMs and Hsp90 are highly sensitive to structural changes. The unique role of HRM7 in heme activation stems from its specific structural environment, not its mere presence. Likewise, the role of Hsp90 in Hap1 activation is dictated by the conformational or structural state of Hap1, not by the mere strength of Hap1-Hsp90 interaction. It appears likely that HRM7 and Hsp90 act together to promote the Hap1 conformational changes that are necessary for Hap1 activation. Such fundamental mechanisms of HRM-Hsp90 cooperation may operate in diverse regulatory systems to mediate signal transduction.
APA, Harvard, Vancouver, ISO, and other styles
6

Xiang, Jianxing, Su Yang, Ning Xin, Marta A. Gaertig, Roger H. Reeves, Shihua Li, and Xiao-Jiang Li. "DYRK1A regulates Hap1–Dcaf7/WDR68 binding with implication for delayed growth in Down syndrome." Proceedings of the National Academy of Sciences 114, no. 7 (January 30, 2017): E1224—E1233. http://dx.doi.org/10.1073/pnas.1614893114.

Full text
Abstract:
Huntingtin-associated protein 1 (Hap1) is known to be critical for postnatal hypothalamic function and growth. Hap1 forms stigmoid bodies (SBs), unique neuronal cytoplasmic inclusions of unknown function that are enriched in hypothalamic neurons. Here we developed a simple strategy to isolate the SB-enriched fraction from mouse brain. By analyzing Hap1 immunoprecipitants from this fraction, we identified a Hap1-interacting SB component, DDB1 and CUL4 associated factor 7 (Dcaf7)/WD40 repeat 68 (WDR68), whose protein level and nuclear translocation are regulated by Hap1. Moreover, we found that Hap1 bound Dcaf7 competitively in cytoplasm with dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A), a protein implicated in Down syndrome (DS). Depleting Hap1 promoted the DYRK1A–Dcaf7 interaction and increased the DYRK1A protein level. Transgenic DS mice overexpressing DYRK1A showed reduced Hap1–Dcaf7 association in the hypothalamus. Furthermore, the overexpression of DYRK1A in the hypothalamus led to delayed growth in postnatal mice, suggesting that DYRK1A regulates the Hap1–Dcaf7 interaction and postnatal growth and that targeting Hap1 or Dcaf7 could ameliorate growth retardation in DS.
APA, Harvard, Vancouver, ISO, and other styles
7

Gong, Yan-Ju, Ying Feng, Yuan-Yuan Cao, Jia Zhao, Wei Wu, Ya-Yun Zheng, Jia-Rui Wu, Xin Li, Gui-Zhi Yang, and Xue Zhou. "Huntingtin-associated protein 1 plays an essential role in the pathogenesis of type 2 diabetes by regulating the translocation of GLUT4 in mouse adipocytes." BMJ Open Diabetes Research & Care 8, no. 1 (October 2020): e001199. http://dx.doi.org/10.1136/bmjdrc-2020-001199.

Full text
Abstract:
ObjectiveGlucose disposal by insulin-responsive tissues maintains the body glucose homeostasis and insulin resistance leads to a risk of developing type 2 diabetes (T2DM). Insulin stimulates the translocation of glucose transporter isoform 4 (GLUT4) vesicles from intracellular compartments to the plasma membrane to facilitate glucose uptake. However, the underlying mechanisms of GLUT4 vesicle translocation are not well defined. Here we show the role of huntingtin-associated protein 1 (HAP1) in GLUT4 translocation in adipocytes and the pathogenesis of T2DM.Research design and methodsThe parameters for glucose metabolism including body weight, glucose tolerance and insulin tolerance were assessed in wild-type (WT) and Hap1+/- mice. HAP1 protein expression was verified in adipose tissue. Hap1 mRNA and protein expression was monitored in adipose tissue of high-fat diet (HFD)-induced diabetic mice. Insulin-stimulated GLUT4 vesicle translocation and glucose uptake were detected using immunofluorescence techniques and quantified in primary adipocytes from Hap1-/- mice. The interaction between HAP1 and GLUT4 was assessed by immunofluorescence colocalization and co-immunoprecipitation in HEK293 cells and adipose tissue. The role of sortilin in HAP1 and GLUT4 interaction was approved by co-immunoprecipitation and RNA interference.ResultsThe expression of Hap1 mRNA and protein was detected in WT mouse adipose tissue and downregulated in adipose tissue of HFD-induced diabetic mice. Hap1+/- mice exhibited increased body weight, pronounced glucose tolerance and significant insulin intolerance compared with the WT mice. HAP1 colocalized with GLUT4 in mouse adipocytes and cotransfected HEK293 cells. Furthermore, the insulin-stimulated GLUT4 vesicle translocation and glucose uptake were defective in Hap1-/- adipocytes. Finally, sortilin mediated the interaction of HAP1 and GLUT4.ConclusionsOur study showed that HAP1 formed a protein complex with GLUT4 and sortilin, and played a critical role in insulin-stimulated GLUT4 translocation in adipocytes. Its downregulation may contribute to the pathogenesis of diabetes.
APA, Harvard, Vancouver, ISO, and other styles
8

Hach, Angela, Thomas Hon, and Li Zhang. "A New Class of Repression Modules Is Critical for Heme Regulation of the Yeast Transcriptional Activator Hap1." Molecular and Cellular Biology 19, no. 6 (June 1, 1999): 4324–33. http://dx.doi.org/10.1128/mcb.19.6.4324.

Full text
Abstract:
ABSTRACTHeme plays key regulatory roles in numerous molecular and cellular processes for systems that sense or use oxygen. In the yeastSaccharomyces cerevisiae, oxygen sensing and heme signaling are mediated by heme activator protein 1 (Hap1). Hap1 contains seven heme-responsive motifs (HRMs): six are clustered in the heme domain, and a seventh is near the activation domain. To determine the functional role of HRMs and to define which parts of Hap1 mediate heme regulation, we carried out a systematic analysis of Hap1 mutants with various regions deleted or mutated. Strikingly, the data show that HRM1 to -6, located in the previously designated Hap1 heme domain, have little impact on heme regulation. All seven HRMs are dispensable for Hap1 repression in the absence of heme, but HRM7 is required for Hap1 activation by heme. More importantly, we show that a novel class of repression modules—RPM1, encompassing residues 245 to 278; RPM2, encompassing residues 1061 to 1185; and RPM3, encompassing residues 203 to 244—is critical for Hap1 repression in the absence of heme. Biochemical analysis indicates that RPMs mediate Hap1 repression, at least partly, by the formation of a previously identified higher-order complex termed the high-molecular-weight complex (HMC), while HRMs mediate heme activation by permitting heme binding and the disassembly of the HMC. These findings provide significant new insights into the molecular interactions critical for Hap1 repression in the absence of heme and Hap1 activation by heme.
APA, Harvard, Vancouver, ISO, and other styles
9

Hickman, Mark J., and Fred Winston. "Heme Levels Switch the Function of Hap1 of Saccharomyces cerevisiae between Transcriptional Activator and Transcriptional Repressor." Molecular and Cellular Biology 27, no. 21 (September 4, 2007): 7414–24. http://dx.doi.org/10.1128/mcb.00887-07.

Full text
Abstract:
ABSTRACT Changes in oxygen levels cause widespread changes in gene expression in organisms ranging from bacteria to humans. In Saccharomyces cerevisiae, this response is mediated in part by Hap1, originally identified as a heme-dependent transcriptional activator that functions during aerobic growth. We show here that Hap1 also plays a significant and direct role under hypoxic conditions, not as an activator, but as a repressor. The repressive activity of Hap1 controls several genes, including three ERG genes required for ergosterol biosynthesis. Chromatin immunoprecipitation experiments showed that Hap1 binds to the ERG gene promoters, while additional experiments showed that the corepressor Tup1/Ssn6 is recruited by Hap1 and is also required for repression. Furthermore, mutational analysis demonstrated that conserved Hap1 binding sites in the ERG5 5′ regulatory region are required for repression. The switch of Hap1 from acting as a hypoxic repressor to an aerobic activator is determined by heme, which is synthesized only in the presence of oxygen. The ability of Hap1 to function as a ligand-dependent repressor and activator is a property shared with mammalian nuclear hormone receptors and likely allows greater transcriptional control by Hap1 in response to changing oxygen levels.
APA, Harvard, Vancouver, ISO, and other styles
10

Hon, Thomas, Hee Chul Lee, Angela Hach, Jill L. Johnson, Elizabeth A. Craig, Hediye Erdjument-Bromage, Paul Tempst, and Li Zhang. "The Hsp70-Ydj1 Molecular Chaperone Represses the Activity of the Heme Activator Protein Hap1 in the Absence of Heme." Molecular and Cellular Biology 21, no. 23 (December 1, 2001): 7923–32. http://dx.doi.org/10.1128/mcb.21.23.7923-7932.2001.

Full text
Abstract:
ABSTRACT In Saccharomyces cerevisiae, heme directly mediates the effects of oxygen on transcription through the heme activator protein Hap1. In the absence of heme, Hap1 is bound by at least four cellular proteins, including Hsp90 and Ydj1, forming a higher-order complex, termed HMC, and its activity is repressed. Here we purified the HMC and showed by mass spectrometry that two previously unidentified major components of the HMC are the Ssa-type Hsp70 molecular chaperone and Sro9 proteins. In vivo functional analysis, combined with biochemical analysis, strongly suggests that Ssa proteins are critical for Hap1 repression in the absence of heme. Ssa may repress the activities of both Hap1 DNA-binding and activation domains. The Ssa cochaperones Ydj1 and Sro9 appear to assist Ssa in Hap1 repression, and only Ydj1 residues 1 to 172 containing the J domain are required for Hap1 repression. Our results suggest that Ssa-Ydj1 and Sro9 act together to mediate Hap1 repression in the absence of heme and that molecular chaperones promote heme regulation of Hap1 by a mechanism distinct from the mechanism of steroid signaling.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "HAP1"

1

Walker, Lisa J. "HAP1 : a human DNA repair enzyme." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386682.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Barzilay, Gil. "Characterisation of human AP endonuclease I (HAP1)." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318791.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Wu, Linyan, and wu0071@flinders edu au. "BRAIN DERIVED NEUROTROPHIC FACTOR TRANSPORT AND PHYSIOLOGICAL SIGNIFICANCE." Flinders University. Medicine, 2007. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20071204.113001.

Full text
Abstract:
Neurotrophins are important signaling molecules in neuronal survival and differentiation. The precursor forms of neurotrophins (proneurotrophins) are the dominant form of gene products in animals, which are cleaved to generate prodomain and mature neurotrophins, and are sorted to constitutive or regulated secretory pathway and released. Brain-derived neurotrophic factor (BDNF) plays a pivotal role in the brain development and in the pathogenesis of neurological diseases. In Huntington’s disease, the defective transport of BDNF in cortical and striatal neurons and the highly expressed polyQ mutant huntingtin (Htt) result in the degeneration of striatal neurons. The underlying mechanism of BDNF transport and release is remains to be investigated. Current studies were conducted to identify the mechanisms of how BDNF is transported in axons post Golgi trafficking. By using affinity purification and 2D-DIGE assay, we show Huntingtin-associated protein 1 (HAP1) interacts with the prodomain and mature BDNF. The GST pull-down assays have addressed that HAP1 directly binds to the prodomain but not to mature BDNF and this binding is decreased by PolyQ Htt. HAP1 immunoprecipitation shows that less proBDNF is associated with HAP1 in the brain homogenate of Huntington’s disease compared to the control. Co-transfections of HAP1 and BDNF plasmids in PC12 cells show HAP1 is colocalized with proBDNF and the prodomain, but not mature BDNF. ProBDNF was accumulated in the proximal and distal segments of crushed sciatic nerve in wild type mice but not in HAP1-/- mice. The activity-dependent release of the prodomain of BDNF is abolished in HAP1-/- mice. We conclude that HAP1 is the cargo-carrying molecule for proBDNF-containing vesicles and plays an essential role in the transport and release of BDNF in neuronal cells. 20-30% of people have a valine to methionine mutation at codon 66 (Val66Met) in the prodomain BDNF, which results in the retardation of transport and release of BDNF, but the mechanism is not known. Here, GST-pull down assays demonstrate that HAP1 binds Val66Met prodomain with less efficiency than the wild type and PolyQ Htt further reduced the binding, but the PC12 cells colocalization rate is almost the same between wt prodomain/HAP1 and Val66Met prodomain/HAP1, suggesting that the mutation in the prodomain may reduce the release by impairing the cargo-carrying efficiency of HAP1, but the mutation does not disrupt the sorting process. Recent studies have shown that proneurotrophins bind p75NTR and sortilin with high affinity, and trigger apoptosis of neurons in vitro. Here, we show that proBDNF plays a role in the death of axotomized sensory neurons. ProBDNF, p75NTR and sortilin are highly expressed in DRG neurons. The recombinant proBDNF induces the dose-dependent death of PC12 cells and the death activity is completely abolished in the presence of antibodies against the prodomain of BDNF. The exogenous proBDNF enhances the death of axotomized sensory neurons and the antibodies to the prodomain or exogenous sortilin-extracellular domain-Fc fusion molecule reduces the death of axotomized sensory neurons. We conclude that proBDNF induces the death of sensory neurons in neonatal rats and the suppression of endogenous proBDNF rescued the death of axotomized sensory neurons.
APA, Harvard, Vancouver, ISO, and other styles
4

Macêdo, Cláudia Souza Macedo. "Caracterização fisiológica de mutantes Kluyveromyces lactis ∆hap1 e ∆rox1 sob aerobiose e hipoxia." Universidade Federal de Viçosa, 2005. http://www.locus.ufv.br/handle/123456789/10694.

Full text
Abstract:
Submitted by Nathália Faria da Silva (nathaliafsilva.ufv@gmail.com) on 2017-06-14T14:43:21Z No. of bitstreams: 1 resumo.pdf: 19226 bytes, checksum: 3311f50c2162c5bb897dc91d378af6b2 (MD5)
Made available in DSpace on 2017-06-14T14:43:21Z (GMT). No. of bitstreams: 1 resumo.pdf: 19226 bytes, checksum: 3311f50c2162c5bb897dc91d378af6b2 (MD5) Previous issue date: 2005-05-15
Conselho Nacional de Desenvolvimento Científico e Tecnológico
Na busca de novos resultados para elucidar o papel de HAP1 e ROX1, que codificam um ativador do metabolismo oxidativo e um repressor do metabolismo oxidorredutivo, respectivamente, na levedura Crabtree negativa Kluyveromyces lactis cuja versatilidade metabólica pode ser explorada em vários campos da biotecnologia, inicialmente, foi identificado um gene ortólogo ROX1 à S. cerevisiae na seqüência genômica de K.lactis. O gene KlROX1 possui 40% de identidade daquele presente em S. cerevisiae e um motif característico do domínio HMG (High Mobility Group). Com base nessa seqüência uma linhagem mutante com deleção de ROX1 foi construída e confirmada. O fenótipo URA + e rox1 - dos transformantes obtidos, K.lactis ∆rox1::URA3, foram 100% estáveis sob condição seletiva. O gene putativo ROX1 de K.lactis teve a sua função em resposta ao oxigênio confirmada em culturas de K. lactis sob regime contínuo e desrepressão por glicose, pois, a deleção de ROX1 induziu a um aumento no nível do transcrito do gene hipóxico HEM13. A análise dos produtos do metabolismo permitiu inferir que a deleção do gene ROX1 em K. lactis aumentou a capacidade fermentativa dessa levedura sob aerobiose e de desrepressão catabólica. A investigação em culturas K. lactis ∆hap1 submetidas ao cultivo contínuo aeróbico sob desrepressão por glicose revelou um fenótipo relacionado ao metabolismo oxidorredutivo, ou seja, K. lactis ∆hap1 é mais fermentativa levando a diversidade de metabólitos em torno do piruvato. A proposta da via de regulação parcial negativa controlando a expressão de HEM13 foi confirmada nas culturas K. lactis.
The objective of this study was to search for new results in order to elucidate the role of HAP1 and ROX1, which codify an oxidative metabolism activator and an oxidoreductive metabolism repressor respectively, in the Crabtree-negative yeast Kluyveromyces lactis, whose metabolic versatility can be exploited in several biotechnology fields. Initially, a ROX1 gene orthologous to S. cerevisiae was identified in the genomic sequence of K. lactis. The KlROX1 gene has 40% identity with the one present in S. cerevisiae and a characteristic motif of the HMG (High Mobility Group) domain. Based on this sequence, a mutant line with ROX1 deletion was built and confirmed. The obtained transformant URA + and rox1 - phenotypes, K. lactis ∆rox1::URA3, were 100% stable under selective condition. The putative K. lactis ROX1 gene had its function in response to oxygen confirmed in cultures of K. lactis under continuous regime and glucose derepression, since ROX1 deletion induced an increase in the level of the HEM13 hypoxic gene transcript. The analysis of metabolism products allowed inferring that the deletion of gene ROX1 in K. lactis increased the yeast fermentative capacity under aerobic and catabolic derepression. The investigation in K. lactis ∆hap1 cultures under continuous aerobic cultivation and glucose derepressiom revealed a phenotype related to oxidoreductive metabolism, in other words, K. lactis ∆hap1 is more fermentative, leading to metabolite diversity around the piruvate. The proposal of the partial negative regulation pathway controlling the HEM13 expression was confirmed in K. lactis cultures.
APA, Harvard, Vancouver, ISO, and other styles
5

DEFRANOUX, NADINE. "Analyse moleculaire du gene cyp1 (hap1) codant pour un regulateur transcriptionnel multifonctionnel de saccharomyces cerevisiae." Paris 7, 1991. http://www.theses.fr/1991PA077157.

Full text
Abstract:
Chez saccharomyces cerevisiae, le regulateur transcriptionnel cyp1 (ha1) module en fonction de l'etat d'oxydo-reduction de la cellule, l'expression de genes codant pour des apohemoproteines ou des enzymes liees a l'utilisation de l'oxygene. Suivant le gene cible et la presence ou l'absence d'heme ou d'oxygene, il se comporte comme un activateur ou comme un represseur. En presence d'heme et d'oxygene, cyp1 se fixe sur des sequences nucleotidiques qui ne presentent pas de consensus bien defini. Ce phenotype complexe pose la question de savoir s'il s'agit d'une proteine a zinc cluster d'autant qu'un residu histidine occupe la position invariable du sixieme residu cysteine indispensable a la formation de la structure. Des souches mutees au locus cyp1 presentant un double phenotype ont ete isolees au laboratoire. Les proteines mutantes discriminent deux sequences cibles peu similaires: l'une de ces cibles n'est plus reconnue alors que pour l'autre non seulement la fixation est preservee mais elle s'accompagne d'une superactivation du gene. Nous avons montre que ce phenotype pleiotrope resulte d'une substitution serine vers arginine (en position 63) situee a la base de la structure a zinc. La fonction de l'acide amine present a cette position a ete extensivement etudie. Nous avons introduit par mutagenese dirigee des mutations faux-sens soit a la position 63, soit au niveau des ligands possibles du zinc. Nos resultats montrent que: 1) cyp1 appartient a la famille des regulateurs a zinc cluster. Un residu cysteine bien que localise a une position inhabituelle par rapport a la sequence consensus, est le sixieme ligand du zinc; 2) la structure zinc cluster est impliquee tant dans la regulation negative que positive, que les cellules soient carencees en heme ou pas; 3) l'acide amine precedant la premiere cysteine du motif appartient a un element qui intervient dans la discrimination des cibles. De plus, la nature de cet acide amine affecte l'efficacite de l'activite regulatrice de cyp1
APA, Harvard, Vancouver, ISO, and other styles
6

Vieira, Nichelle Antunes. "Caracterização de células humanas Hap1 nocaute para FBXO25: via de sinalização da ERK quinase e proliferação celular." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17131/tde-25042018-143544/.

Full text
Abstract:
A proteína FBXO25 é uma E3-ligase do tipo SCF, responsável pela seletividade da ligação da Ub à proteína substrato e pelo direcionamento da proteína marcada para o barril proteassomal 26s. Sabe-se que FBXO25 é capaz de interagir e ubiquitinar a proteína Elk-1 em células HEK293T e, assim, inibir a expressão de genes importantes na regulação da proliferação celular, como C-FOS e EGR-1, após estímulo com o mitógeno PMA. Aqui mostramos que FBXO25 atua em um outro ponto da via das MAPKs, modulando os níveis de fosforilação de ERK1/2. Por meio da utilização de células nocaute para FBXO25 (FBXO25KO) foi possível observar que o tratamento com PMA promoveu aumento dos níveis de fosforilação de ERK1/2 nestas células quando comparadas com sua linhagem parental. Observouse também que o estímulo com os mitógenos PMA ou ATP levou a um aumento da proliferação celular não relacionada à modulação direta do ciclo celular nas células nocautes, sendo que estas apresentaram uma redução significativa dos seus níveis de apoptose. Tomando esses resultados em conjunto, mostramos que FBXO25 atua sobre a sinalização de MAPK por meio de redução da ativação ERK1/2 e, dessa forma, promove uma resposta secundária sobre o fenótipo de proliferação celular
The FBXO25 protein is an SCF-type E3-ligase responsible for the selectivity of Ub binding to the protein and the targeting of the labeled protein to the 26s proteasome barrel. FBXO25 has been long known to be able to interact and ubiquitinate the Elk-1 protein in HEK293T cells, thereby inducing a decrease in the expression of important genes in the regulation of cell proliferation such as CFOS and EGR-1 after stimulation with the mitogen PMA. Here we show that FBXO25 acts at another point in the MAPK pathway by modulating the ERK1/2 phosphorylation levels. We observed that the treatment with PMA rised the phosphorylated levels of ERK1/2 in knockout cells for FBXO25 (FBXO25KO) when compared to its parental lineage. Stimulation with the mitogens PMA or ATP also led to an increase in cell proliferation unrelated to a direct modulation of the cell cycle in knockout cells, with a significant weight of apoptosis levels being observed. Taking these results together, we show that FBXO25 acts on MAPK signaling by reducing ERK1/2 activation and thus promotes a secondary response on the cell proliferation phenotype.
APA, Harvard, Vancouver, ISO, and other styles
7

Capps, Denise. "The Regulation of NAP4 in Saccharomyces cerevisiae." ScholarWorks@UNO, 2011. http://scholarworks.uno.edu/td/116.

Full text
Abstract:
The CCAAT binding-factor (CBF) is a transcriptional activator conserved in eukaryotes. The CBF in Saccharomyces cerevisiae is a multimeric heteromer termed the Hap2/3/4/5 complex. Hap4, which contains the activation domain of the complex, is also the regulatory subunit and is known to be transcriptionally controlled by carbon sources. However, little is known about Hap4 regulation. In this report, I identify mechanisms by which Hap4 is regulated, including: (1) transcriptional regulation via two short upstream open reading frames (uORFs) in the 5' leader sequence of HAP4 mRNA; (2) proteasome-dependent degradation of Hap4; and (3) identification of two negative regulators of HAP4 expression, CYC8 and SIN4. I also report differential patterns of Hap4 cellular localization which depends on (1) carbon sources, (2) abundance of Hap4 protein, and (3) presence or absence of mitochondrial DNA (mtDNA).
APA, Harvard, Vancouver, ISO, and other styles
8

Mejia, Luis Antonio. "Interaction Proteomics of Autism Spectrum Disorder- and Intellectual Disability-Associated Proteins Identifies a Novel Hap1-Tsc1 Signaling Link that Controls Neuronal mTORC1 Signaling and Pyramidal Neuron Morphogenesis." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11190.

Full text
Abstract:
Autism spectrum disorder (ASD) and intellectual disability (ID) are neurodevelopmental disorders of cognition that remain incompletely understood. Here, using a computation-assisted interaction proteomics approach in neural cells including primary neurons, we isolate high-confidence binding partners of proteins linked to ASD and ID. As part of these studies, we uncover the brain-enriched, coiled-coil domain protein huntingtin-associated protein 1 (Hap1) as a novel functional binding partner of the tuberous sclerosis complex (TSC) protein Tsc1. We validate and map the Hap1-Tsc1 interaction, and find that Hap1 and Tsc1 form a complex endogenously in the brain. Hap1 knockdown in primary hippocampal neurons triggers the specification of supernumerary axons, and in utero knockdown of Hap1 in mice profoundly impairs the positioning of pyramidal neurons in the hippocampus in vivo. Importantly, the Hap1 knockdown-induced phenotypes in primary neurons and in vivo recapitulate the phenotypes induced by Tsc1 knockdown. We also define a mechanism by which Hap1 regulates Tsc1 function. We observed that exogenous Hap1 promotes the abundance of soluble, stable Tsc1 expressed in cells. Hap1 knockdown in neurons reduces Tsc1 abundance and accordingly stimulates the activity of mTORC1, as reflected by phosphorylation of the ribosomal protein S6. Importantly, inhibition of mTORC1 signaling suppresses the Hap1 knockdown-induced axon phenotype in hippocampal neurons. Collectively, these findings define a novel relationship between Hap1 and Tsc1 that regulates neuronal Tsc1 abundance, pyramidal neuron development, and neuronal mTORC1 signaling, with important mechanistic implications for our understanding of neurodevelopmental disorders of cognition.
APA, Harvard, Vancouver, ISO, and other styles
9

Hunter, Arielle Ruth. "Characterization of Ubiquitin/Proteasome-Dependent Regulation of Hap2/3/4/5 Complex In Saccharomyces cerevisiae." ScholarWorks@UNO, 2012. http://scholarworks.uno.edu/honors_theses/13.

Full text
Abstract:
The Hap2/3/4/5 complex is a heme-activated, CCAATT binding, global transcriptional activator of genes involved in respiration and mitochondrial biogenesis in the yeast species Saccharomyces cerevisiae. Hap4 is the regulatory subunit of the complex and its levelsdetermine the activity of the complex. Hap4 is known to play a signaling role in response toenvironmental conditions; however, little is known about the regulation of Hap4 levels or how it responses to a cell’s functional state. The activity of the Hap2-5 complex is known to be reduced in respiratory-deficient cells. In Liu Lab, it has previously been found that a link between Hap4 stability, mediated through 26S proteasome-dependent degradation, and dependence on mitochondrial functional state plays a regulatory role on downstream targets of the Hap complex. However, the mechanism behind this regulation is still largely unknown. In normally functioning yeast cells, Hap4 is a highly unstable protein with a half-life of ~10 min. We have observed that loss of mitochondrial DNA in respiratory deficient rho 0 cells has a role in the further destabilization of Hap4 to a half-life of ~4 min through the ubiquitin-proteasome pathway. Through the screening of a collection of mutants defective in E2 ubiquitin-conjugating enzymes, we show that Hap4 is greatly stabilized in ubc1Δubc4Δ double mutant cells. We also show that Hap4 stabilization in the ubc1Δubc4Δ mutant leads to increased activity of the Hap2-5 complex, indicating that mitochondrial biogenesis in yeast is regulated by the functional state of mitochondria through ubiquitin/proteasome-dependent degradation of Hap4. Furthermore, studies on Hap4 mutants involving two highly conserved cysteine residues led to a proposed mechanism behind the regulation of Ubc4 activity towards Hap4 in response to changes in the cellular redox state.
APA, Harvard, Vancouver, ISO, and other styles
10

Higgins, Robert Francis 1962. "Hercules attitude processor (HAP)." Diss., Virginia Tech, 1992. http://hdl.handle.net/10919/38349.

Full text
Abstract:
The design and analysis of a microprocessor-based gyro attitude data processing system used to geolocate natural phenomena from space was performed. Operational software was written and a HERCULES Attitude Processor (HAP) unit was built and tested. Strict adherence to worst-case timing design criterion was a prime hardware design consideration. Weight, volume, and power requirements were also addressed. Redundancy was included for critical time maintenance functions. Hardware performance and accuracy was calculated and measured. Operational software was written to control the functions of the HAP unit. Algorithms were written to accurately process the high speed gyro attitude data. Data communication between subsystems in the HERCULES system was controlled by the software. Subsystem configuration, operating modes, self-testing, and resource management was performed by the operational software. Testing was performed on the HAP unit and operational software. Hardware and software performance was analyzed and is presented.
Ph. D.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "HAP1"

1

Herring, Christopher. Studies on the DNA repair protein HAP1. Manchester: University of Manchester, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Sud, Kanika. Practical hapi. Berkeley, CA: Apress, 2020. http://dx.doi.org/10.1007/978-1-4842-5805-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Zanzibar hapo kale. Zanzibar, Tanzania: Masomo Bookshop [distributor], 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Hap kujo. Sŏul-si: Uri Munhwa, 2007.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Grieshaber, Helmut A. P. HAP Grieshaber. [Stuttgart]: Staatsgalerie Stuttgart, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Wornell, Paul. HAPM component life manual. London: Spon, 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Hapa girl: A memoir. Philadelphia, PA: Temple University Press, 2007.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Valk, Barbara G. HAPI thesaurus, 1970-1994. [Los Angeles]: UCLA Latin American Center Publications, University of California, Los Angeles, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Part Asian, 100% Hapa. San Francisco: Chronicle Books, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Naz, Mina. Hape kanch ki churian. Lahore: Maktaba Alq, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "HAP1"

1

Sud, Kanika. "Understanding REST APIs." In Practical hapi, 1–11. Berkeley, CA: Apress, 2020. http://dx.doi.org/10.1007/978-1-4842-5805-7_1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Sud, Kanika. "Beginning Node.JS." In Practical hapi, 13–19. Berkeley, CA: Apress, 2020. http://dx.doi.org/10.1007/978-1-4842-5805-7_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Sud, Kanika. "Asynchronous JavaScript." In Practical hapi, 21–33. Berkeley, CA: Apress, 2020. http://dx.doi.org/10.1007/978-1-4842-5805-7_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Sud, Kanika. "Your First hapi Application." In Practical hapi, 35–47. Berkeley, CA: Apress, 2020. http://dx.doi.org/10.1007/978-1-4842-5805-7_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Sud, Kanika. "Building on the Basics: Validation, Authentication, and Plugins." In Practical hapi, 49–62. Berkeley, CA: Apress, 2020. http://dx.doi.org/10.1007/978-1-4842-5805-7_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Sud, Kanika. "Capstone Project: REST API for Polling App." In Practical hapi, 85–115. Berkeley, CA: Apress, 2020. http://dx.doi.org/10.1007/978-1-4842-5805-7_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Sud, Kanika. "Database Connectivity." In Practical hapi, 63–84. Berkeley, CA: Apress, 2020. http://dx.doi.org/10.1007/978-1-4842-5805-7_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Metze, Dieter, Vanessa F. Cury, Ricardo S. Gomez, Luiz Marco, Dror Robinson, Eitan Melamed, Alexander K. C. Leung, et al. "HAPE." In Encyclopedia of Molecular Mechanisms of Disease, 774. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7636.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Metze, Dieter, Vanessa F. Cury, Ricardo S. Gomez, Luiz Marco, Dror Robinson, Eitan Melamed, Alexander K. C. Leung, et al. "HAPO." In Encyclopedia of Molecular Mechanisms of Disease, 774. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7637.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Webster, Steven. "The Tamaikoha Hapū Branch: Hapū Affiliations." In A Separate Authority (He Mana Motuhake), Volume I, 141–74. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41042-1_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "HAP1"

1

Gerhards, Nora M., Charlotte Guyader, Vincent A. Blomen, Aslı Küçükosmanoğlu, Olaf van Tellingen, Daniel J. Vis, Lodewyk F. Wessels, Thijn R. Brummelkamp, Piet Borst, and Sven Rottenberg. "Abstract 3607: Loss-of-function screens using haploid KBM7 and HAP1 cells to identify mechanisms of anti-cancer drug resistance." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3607.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Kurtin, Philip S., Joost P. H. M. Hausmans, and Marco J. G. Bekooij. "HAPI." In SCOPES '16: 19th International Workshop on Software and Compilers for Embedded Systems. New York, NY, USA: ACM, 2016. http://dx.doi.org/10.1145/2906363.2906381.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Aly, Heba, and Ashok Agrawala. "Hapi." In MobiQuitous '18: Computing, Networking and Services. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3286978.3286980.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Laskaridis, Stefanos, Stylianos I. Venieris, Hyeji Kim, and Nicholas D. Lane. "HAPI." In ICCAD '20: IEEE/ACM International Conference on Computer-Aided Design. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3400302.3415698.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Choudhury, Olivia, Ankush Chakrabarty, and Scott J. Emrich. "HAPI-Gen." In BCB '16: ACM International Conference on Bioinformatics, Computational Biology, and Health Informatics. New York, NY, USA: ACM, 2016. http://dx.doi.org/10.1145/2975167.2975175.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Nia, Masoud Mohebbi, and Tharek A. Rahman. "Fixed satellite service (FSS) and high altitude platform (HAP) interference assessment for adjacent channels inside HAPS coverage area." In 2011 Fourth International Conference on Modeling, Simulation and Applied Optimization (ICMSAO). IEEE, 2011. http://dx.doi.org/10.1109/icmsao.2011.5775463.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Lin, Ying-Dar Jason, Tzu-Chieh Tsai, San-Chiao Huang, and Mario Gerla. "HAP." In Conference proceedings. New York, New York, USA: ACM Press, 1993. http://dx.doi.org/10.1145/166237.166258.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Chen, Xinlei, Xiangxiang Xu, Xinyu Liu, Hae Young Noh, Lin Zhang, and Pei Zhang. "HAP." In SenSys '16: The 14th ACM Conference on Embedded Network Sensor Systems. New York, NY, USA: ACM, 2016. http://dx.doi.org/10.1145/2994551.2996694.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Fujisaki, Kazuhiro, Shigeru Tadano, and Naoki Sasaki. "Bone Tissue Strain and Lattice Strain of HAp Crystals Under Tensile Loading." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-59253.

Full text
Abstract:
Bone tissue is a composite material composed of hydroxyapatite (HAp) and collagen. Because HAp in bone tissue is a crystal structure, the X-ray diffraction method is available to measure the lattice strain of HAp. A relationship between macroscopic bone tissue strain and lattice strain of HAp in a bone specimen was investigated using X-ray strain measurement under tensile loading. The strip specimens were cut from cortical bone in a shaft of bovine femur. As a result, lattice strains of HAp showed lower value than the bone tissue strain. The strain ratio of the HAp crystals to the bone tissue was formulated with an elastic modulus and volume fraction of HAp in the bone tissue.
APA, Harvard, Vancouver, ISO, and other styles
10

Dubey, Manisha, P. K. Srijith, and Maunendra Sankar Desarkar. "HAP-SAP." In SIGSPATIAL '20: 28th International Conference on Advances in Geographic Information Systems. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3397536.3422233.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "HAP1"

1

Harrison, C. D., D. J. Akers, and C. E. ,. Jr Raleigh. HAPs-RX(TM). Office of Scientific and Technical Information (OSTI), July 1997. http://dx.doi.org/10.2172/16508.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

David J. Akers and Clifford E. Raleigh. HAPs-Rx: Precombustion Removal of Hazardous Air Pollutant Precursors. Office of Scientific and Technical Information (OSTI), March 1998. http://dx.doi.org/10.2172/899956.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Michael R. Milota : Kaichang Li. VOC and HAP recovery using ionic liquids. Office of Scientific and Technical Information (OSTI), May 2007. http://dx.doi.org/10.2172/909870.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Olson, Gregory J. Biochemical Removal of HAP Precursors from Coal. Office of Scientific and Technical Information (OSTI), May 1997. http://dx.doi.org/10.2172/2094.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Edmond, W. Host Access Protocol (HAP) specification: Version 2. RFC Editor, April 1991. http://dx.doi.org/10.17487/rfc1221.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Olson, G., L. Tucker, and J. Richards. Biochemical Removal of HAP Precursors From Coal. Office of Scientific and Technical Information (OSTI), July 1997. http://dx.doi.org/10.2172/620969.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Kyriakis, John M. The Role of HAP Kinases in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 1995. http://dx.doi.org/10.21236/ada300037.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Benson, S. A., T. A. Erickson, and D. W. Brekke. Comparison of HAPs from advanced and conventional power systems: Tidd versus Cardinal. Office of Scientific and Technical Information (OSTI), November 1995. http://dx.doi.org/10.2172/125008.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Faulise, Angelique L. Operational Leadership: Operational Art and General H. H. 'Hap' Arnold. Fort Belvoir, VA: Defense Technical Information Center, February 1997. http://dx.doi.org/10.21236/ada325022.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

La Scala, John, Steven Boyd, Kevin Andrews, Terese Glodek, Caroline Lochner, Philip Myers, Felecia Levine, Daniel De Bonis, Robert Hayes, and James Sands. Low-Hazardous Air Pollutant (HAP)/Volatile Organic Compound (VOC) - Compliant Resins for Military Applications. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada577082.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'HAP1' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography