Gotowe bibliografie tematyczne / Novel Human Protein Family

Gotowa bibliografia na temat „Novel Human Protein Family”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 20 lutego 2023

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Artykuły w czasopismach na temat "Novel Human Protein Family"

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Elbadawy, Mohamed, Tatsuya Usui, Hideyuki Yamawaki i Kazuaki Sasaki. "Novel Functions of Death-Associated Protein Kinases through Mitogen-Activated Protein Kinase-Related Signals". International Journal of Molecular Sciences 19, nr 10 (4.10.2018): 3031. http://dx.doi.org/10.3390/ijms19103031.

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Death associated protein kinase (DAPK) is a calcium/calmodulin-regulated serine/threonine kinase; its main function is to regulate cell death. DAPK family proteins consist of DAPK1, DAPK2, DAPK3, DAPK-related apoptosis-inducing protein kinases (DRAK)-1 and DRAK-2. In this review, we discuss the roles and regulatory mechanisms of DAPK family members and their relevance to diseases. Furthermore, a special focus is given to several reports describing cross-talks between DAPKs and mitogen-activated protein kinases (MAPK) family members in various pathologies. We also discuss small molecule inhibitors of DAPKs and their potential as therapeutic targets against human diseases.
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Davis, Beckley, Aaron Tocker, Suzanna Talento i Kimberly Jacob. "Identification of a novel protein protein interaction pathway with NLRC3 (INM2P.359)". Journal of Immunology 194, nr 1_Supplement (1.05.2015): 126.12. http://dx.doi.org/10.4049/jimmunol.194.supp.126.12.

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Abstract Nucleotide binding domain, leucine rich repeat CARD containing protein 3 (NLRC3) is a member of the NLR gene family. Members of this family have been associated with human inflammatory diseases such as Crohn’s disease and cryopyrin-associated periodic syndrome. Although NLRC3 (and others) are not associated with human diseases, it is expressed preferentially in the immune system and functions in pathogen recognition. NLRC3 is an intracellular protein involved in the sensing of lipopolysaccharide and cytosolic nucleic acids. NLRC3 is hypothesized to act as a negative regulator in response to bacterial and viral infection, suggesting that the vertebrate immune system has evolved specific inhibitors to limit the inflammatory response. We performed an unbiased yeast two-hybrid screen using an amino terminal fragment of NLRC3 to identify putative interacting proteins that might help elucidate the mechanism by which NLRC3 might inhibit inflammatory responses. To this end, we identified several interacting proteins. One protein in particular acts as a scaffold important in regulating the cytoskeleton, cell adhesion and proliferation. Structure function analysis has localized the domains necessary and sufficient for interacting with NLRC3. Additionally, confocal microscopy demonstrates that these two proteins colocalize in transformed human epithelial cells. This data suggests that NLRC3 interacts specifically with a novel scaffold.
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Guignard, F., J. Mauel i M. Markert. "Identification and characterization of a novel human neutrophil protein related to the S100 family". Biochemical Journal 309, nr 2 (15.07.1995): 395–401. http://dx.doi.org/10.1042/bj3090395.

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A rabbit polyclonal antibody raised against myeloid-related protein 8 (MRP-8), a protein of the S100 family, recognized another S100 protein (MRP-14) as well as a protein of 6.5 kDa (p6) in the cytosol of resting neutrophils. p6 was found to be a novel member of the S100 family. It consisted of two isoforms with pI values of 6.2 (the minor form, p6a) and 6.3 (the major form, p6b) and constituted 5% of the total cytosolic proteins. Both isoforms were also demonstrated in the cytosol of monocytes, but not in lymphocytes, as previously shown for MRP-8 and MRP-14. Only the major isoform bound radioactive Ca2+, as also observed for MRP-8, whereas the different variants of MRP-14 were all labelled. On neutrophil activation with opsonized zymosan, a stimulant known to require extracellular Ca2+, 58% of p6a and 42% of p6b was translocated to the membrane. With phorbol 12-myristate 13-acetate, a Ca(2+)-independent stimulant, no translocation was detected. This translocation pattern was similar to that observed with MRP-8 and MRP-14. In addition, p6, MRP-8 and MRP-14 were specifically associated with the cytoskeletal fraction of the membrane. The Ca(2+)-dependent translocation of the novel S100 protein in parallel with MRP-8 and MRP-14 suggests a role for these proteins in regulating the Ca2+ signal to the membrane cytoskeleton and thus in regulating neutrophil activation.
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Singh, Mahendra K., Disha Dadke, Emmanuelle Nicolas, Ilya G. Serebriiskii, Sinoula Apostolou, Adrian Canutescu, Brian L. Egleston i Erica A. Golemis. "A Novel Cas Family Member, HEPL, Regulates FAK and Cell Spreading". Molecular Biology of the Cell 19, nr 4 (kwiecień 2008): 1627–36. http://dx.doi.org/10.1091/mbc.e07-09-0953.

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For over a decade, p130Cas/BCAR1, HEF1/NEDD9/Cas-L, and Efs/Sin have defined the Cas (Crk-associated substrate) scaffolding protein family. Cas proteins mediate integrin-dependent signals at focal adhesions, regulating cell invasion and survival; at least one family member, HEF1, regulates mitosis. We here report a previously undescribed novel branch of the Cas protein family, designated HEPL (for HEF1-Efs-p130Cas-like). The HEPL branch is evolutionarily conserved through jawed vertebrates, and HEPL is found in some species lacking other members of the Cas family. The human HEPL mRNA and protein are selectively expressed in specific primary tissues and cancer cell lines, and HEPL maintains Cas family function in localization to focal adhesions, as well as regulation of FAK activity, focal adhesion integrity, and cell spreading. It has recently been demonstrated that upregulation of HEF1 expression marks and induces metastasis, whereas high endogenous levels of p130Cas are associated with poor prognosis in breast cancer, emphasizing the clinical relevance of Cas proteins. Better understanding of the complete protein family should help inform prediction of cancer incidence and prognosis.
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Li, Xin, Lei Chen, Chaoneng Ji, Bing Liu, Jiefeng Gu, Jian Xu, Xianqiong Zou, Shaohua Gu i Yumin Mao. "Isolation and expression pattern of RGS21 gene, a novel RGS member." Acta Biochimica Polonica 52, nr 4 (8.09.2005): 943–46. http://dx.doi.org/10.18388/abp.2005_3412.

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Regulators of G-protein signaling (RGS) proteins are known for the RGS domain that is composed of a conserved stretch of 120 amino acids, which binds directly to activated G-protein alpha subunits and acts as a GTPase-activating protein (GAP), leading to their deactivation and termination of downstream signals. In this study, a novel human RGS cDNA (RGS21), 1795 bp long and encoding a 152-amino acid polypeptide, was isolated by large-scale sequencing analysis of a human fetal brain cDNA library. Unlike other RGS family members, RGS21 gene has no additional domain/motif and may represent the smallest known member of RGS family. It may belong to the B/R4 subfamily, which suggests that it may serve exclusively as a negative regulator of alphai/o family members and/or alphaq/11. PCR analysis showed that RGS21 mRNA was expressed ubiquitously in the 16 tissues examined, implying general physiological roles.
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Rakowicz-Szulczynska, Ewa M., David G. McIntosh, Peter Morris i McClure Smith. "Novel Family of Gynecologic Cancer Antigens Detected by Anti-HIV Antibody". Infectious Diseases in Obstetrics and Gynecology 2, nr 4 (1994): 171–78. http://dx.doi.org/10.1155/s1064744994000608.

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Objective:The reactivity of gynecologic cancer proteins with monoclonal antibody (MAb) directed against the human immunodeficiency virus I (HIV-I) was tested.Methods:Cytoplasmic and nuclear proteins, extracted from a broad range of gynecologic cancers obtained during standard surgical procedures, were tested in Western blotting with MAb 5023 developed against the amino acid sequences 308–322 of the envelope protein gp120 of HIV-I.Results:Three cell membrane proteins,Mrl20,000 (p120),Mr41,000 (p41), andMr24,000 (p24), and one chromatin protein,Mr24,000 (p24), were detected by MAb 5023 in invasive, poorly differentiated cervical squamous-cell carcinoma; ovarian serous cystadenocarcinoma; poorly and well-differentiated endometrial carcinoma; vulvar squamous-cell carcinoma; and malignant mixed müllerian tumor. The same antigens were identified in cervical carcinoma cell line SiHa. Neither p120 nor p24 was recognized by other MAbs directed against the variable loop of gp120. Antigens p120 and p41 were undetectable in normal ovarian tissue and in biopsy samples of normal vaginal and rectal mucosa. Rectosigmoid cancer as well as colon carcinoma, lung carcinoma, and melanoma cell lines all tested negative.Conclusions:The identified antigens may represent either the products of human genes (proto-onc-ogenes) or, more likely, the products of an unknown virus specifically expressed in female cancer.
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Suk, Kyoungho, Sunshin Kim, Yun-Hee Kim, Seung-Hoon Oh, Moon-Kyu Lee, Kwang-Won Kim, Hee-Dai Kim, Yeon-Soo Seo i Myung-Shik Lee. "Identification of a novel human member of the DEAD box protein family". Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1501, nr 1 (kwiecień 2000): 63–69. http://dx.doi.org/10.1016/s0925-4439(00)00010-7.

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Lev, Sima, John Hernandez, Ricardo Martinez, Alon Chen, Greg Plowman i Joseph Schlessinger. "Identification of a Novel Family of Targets of PYK2 Related to Drosophila Retinal Degeneration B (rdgB) Protein". Molecular and Cellular Biology 19, nr 3 (1.03.1999): 2278–88. http://dx.doi.org/10.1128/mcb.19.3.2278.

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ABSTRACT The protein tyrosine kinase PYK2 has been implicated in signaling pathways activated by G-protein-coupled receptors, intracellular calcium, and stress signals. Here we describe the molecular cloning and characterization of a novel family of PYK2-binding proteins designated Nirs (PYK2 N-terminal domain-interacting receptors). The three Nir proteins (Nir1, Nir2, and Nir3) bind to the amino-terminal domain of PYK2 via a conserved sequence motif located in the carboxy terminus. The primary structures of Nirs reveal six putative transmembrane domains, a region homologous to phosphatidylinositol (PI) transfer protein, and an acidic domain. The Nir proteins are the human homologues of the Drosophila retinal degeneration B protein (rdgB), a protein implicated in the visual transduction pathway in flies. We demonstrate that Nirs are calcium-binding proteins that exhibit PI transfer activity in vivo. Activation of PYK2 by agents that elevate intracellular calcium or by phorbol ester induce tyrosine phosphorylation of Nirs. Moreover, PYK2 and Nirs exhibit similar expression patterns in several regions of the brain and retina. In addition, PYK2-Nir complexes are detected in lysates prepared from cultured cells or from brain tissues. Finally, the Nir1-encoding gene is located at human chromosome 17p13.1, in proximity to a locus responsible for several human retinal diseases. We propose that the Nir and rdgB proteins represent a new family of evolutionarily conserved PYK2-binding proteins that play a role in the control of calcium and phosphoinositide metabolism downstream of G-protein-coupled receptors.
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Sellers, Robert A., David L. Robertson i May Tassabehji. "Ancestry of the AUTS2 family–A novel group of polycomb-complex proteins involved in human neurological disease". PLOS ONE 15, nr 12 (11.12.2020): e0232101. http://dx.doi.org/10.1371/journal.pone.0232101.

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Autism susceptibility candidate 2 (AUTS2) is a neurodevelopmental regulator associated with an autosomal dominant intellectual disability syndrome, AUTS2 syndrome, and is implicated as an important gene in human-specific evolution. AUTS2 exists as part of a tripartite gene family, the AUTS2 family, which includes two relatively undefined proteins, Fibrosin (FBRS) and Fibrosin-like protein 1 (FBRSL1). Evolutionary ancestors of AUTS2 have not been formally identified outside of the Animalia clade. A Drosophila melanogaster protein, Tay bridge, with a role in neurodevelopment, has been shown to display limited similarity to the C-terminal of AUTS2, suggesting that evolutionary ancestors of the AUTS2 family may exist within other Protostome lineages. Here we present an evolutionary analysis of the AUTS2 family, which highlights ancestral homologs of AUTS2 in multiple Protostome species, implicates AUTS2 as the closest human relative to the progenitor of the AUTS2 family, and demonstrates that Tay bridge is a divergent ortholog of the ancestral AUTS2 progenitor gene. We also define regions of high relative sequence identity, with potential functional significance, shared by the extended AUTS2 protein family. Using structural predictions coupled with sequence conservation and human variant data from 15,708 individuals, a putative domain structure for AUTS2 was produced that can be used to aid interpretation of the consequences of nucleotide variation on protein structure and function in human disease. To assess the role of AUTS2 in human-specific evolution, we recalculated allele frequencies at previously identified human derived sites using large population genome data, and show a high prevalence of ancestral alleles, suggesting that AUTS2 may not be a rapidly evolving gene, as previously thought.
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Skeiky, Y. A., D. R. Benson, J. A. Guderian, P. R. Sleath, M. Parsons i S. G. Reed. "Trypanosoma cruzi acidic ribosomal P protein gene family. Novel P proteins encoding unusual cross-reactive epitopes." Journal of Immunology 151, nr 10 (15.11.1993): 5504–15. http://dx.doi.org/10.4049/jimmunol.151.10.5504.

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Abstract We have cloned and characterized cDNA molecules that encode members of the acidic ribosomal protein family (TcP proteins) from the protozoan parasite Trypanosoma cruzi. These proteins have been shown to be antigenic in individuals with T. cruzi infection. Unlike other known eukaryotic cells, T. cruzi possesses at least four types of P protein genes TcP0, TcP1, TcP2a, and TcP2b, each of which is present in multiple copies in the genome. These genes are present on at least three different chromosomes. Although the abundance of TcP0, TcP2a, and TcP2b transcripts do not appear to vary among the parasite life-cycle stages, TcP1 is predominantly expressed in the epimastigote (insect) stage. TcP0 has a C-terminal heptapeptide sequence that is similar to those of archaebacterial acidic (P-like) proteins, but the TcP1/P2 proteins terminate with a shared sequence characteristic of the P proteins of higher eukaryotes. The serine residues or other potential phosphorylation sites typically found within the highly charged C-terminal acidic domain are absent in T. cruzi P proteins. Using synthetic peptides, we demonstrated that approximately 80% of T. cruzi-infected individuals produce two distinct but cross-reactive anti-P antibody specificities directed against the C-termini of TcP0 and TcP1/P2. We also expressed the full length (non-fusion) recombinant human P0 and demonstrated that the T. cruzi anti-P antibodies cross-react with the C-terminal residues of human P-proteins. Conversely, human anti-P protein antibodies in sera from patients with SLE cross-react with the C-terminal epitope of T. cruzi TcP1/P2 proteins. The cross-reactivity of anti-TcP antibodies with human P proteins suggests that, through antigenic conservation, TcP proteins may contribute to the development of autoreactive antibodies in Chagas' disease patients.
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Rozprawy doktorskie na temat "Novel Human Protein Family"

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Cloonan, Nicole, i N/A. "Sin1 and Sin1 Isoforms: An Investigation into the Biological Significance of a Novel Human Protein Family". Griffith University. School of Biomolecular and Biomedical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20071102.150237.

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Stress activated protein kinase (SAPK) interacting protein 1 (Sin1) is a member of a recently characterized gene family, conserved from yeast to humans. The gene copy number is strictly conserved (one Sin1 gene per genome), and the protein may be expressed ubiquitously in mammalian tissues. The Sin1 family has been implicated in several different signal transduction pathways. Originally identified as a partial cDNA and candidate Ras inhibitor, recent functional studies have revealed interactions with an interferon (IFN) receptor subunit (IFNAR2), and the SAPK JNK. Interactions have also been described between the yeast orthologues and the phosphatidylinositol kinase TOR2. Collectively, these data suggest that Sin1 has an important cellular role, and this study has investigated possible functions for this protein. As human Sin1 proteins have no paralogues within the genome, secondary structure homology was used to identify major domains within the protein. Four major domains within human Sin1 were deduced: an N-terminal domain containing a functional nuclear localization signal, a functional nuclear export signal, and a coiledcoil region; the conserved region in the middle that is likely to be a ubiquitin-like β-grasp protein binding domain; a Ras binding domain; and a pleckstrin homology-like domain that targets Sin1 to the plasma membrane and lipid rafts in vivo. Full and partial length EGFP constructs were used to examine the localization of human Sin1, and several isoforms derived from alternative splicing. All isoforms localized to the nucleus and nucleolus. Beyond this, Sin1α and Sin1ϒ had cytoplasmic staining, while Sin1 and Sin1β were also found at the plasma membrane and lipid rafts. Both the N-terminal domain and the conserved region in the middle were found to contribute to nuclear localization. Comparative genomic analysis between human, mouse, rat, dog, and chicken Sin1 genes revealed a number of conserved intronic regions, and the putative functions of these were predicted. Additionally, a putative promoter module within a CpG island and encompassing the transcription start site was predicted in all species. The human CpG island was found to have promoter activity in HEK293 cells. Using bioinformatics, genes that may be co-regulated with Sin1 were identified. These genes contained the Sin1 promoter module, and were found to co-express in large scale gene expression studies. Most of these genes were directly involved in the cellular response to pathogen infection, suggesting a conserved role for Sin1 in this pathway. Key biochemical functions of the Sin1 proteins were also identified, including the ability of Sin1 proteins to form dimers, and the ability of over-expressed Sin1 to induce apoptosis (mediated through the conserved region in the middle). Additionally, endogenous Sin1 protein levels were found to change following serum deprivation and hypoosmotic stress. Together, these studies have provided significant insight into the cellular role of Sin1, suggesting a role in inducing apoptosis as part of the IFN response to viral infection. The biological significance of the Sin1 proteins is discussed in the context of their predicted functions and the evolution of the protein family.
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Cloonan, Nicole. "Sin1 and Sin1 Isoforms: An Investigation into the Biological Significance of a Novel Human Protein Family". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/367210.

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Stress activated protein kinase (SAPK) interacting protein 1 (Sin1) is a member of a recently characterized gene family, conserved from yeast to humans. The gene copy number is strictly conserved (one Sin1 gene per genome), and the protein may be expressed ubiquitously in mammalian tissues. The Sin1 family has been implicated in several different signal transduction pathways. Originally identified as a partial cDNA and candidate Ras inhibitor, recent functional studies have revealed interactions with an interferon (IFN) receptor subunit (IFNAR2), and the SAPK JNK. Interactions have also been described between the yeast orthologues and the phosphatidylinositol kinase TOR2. Collectively, these data suggest that Sin1 has an important cellular role, and this study has investigated possible functions for this protein. As human Sin1 proteins have no paralogues within the genome, secondary structure homology was used to identify major domains within the protein. Four major domains within human Sin1 were deduced: an N-terminal domain containing a functional nuclear localization signal, a functional nuclear export signal, and a coiledcoil region; the conserved region in the middle that is likely to be a ubiquitin-like β-grasp protein binding domain; a Ras binding domain; and a pleckstrin homology-like domain that targets Sin1 to the plasma membrane and lipid rafts in vivo. Full and partial length EGFP constructs were used to examine the localization of human Sin1, and several isoforms derived from alternative splicing. All isoforms localized to the nucleus and nucleolus. Beyond this, Sin1α and Sin1ϒ had cytoplasmic staining, while Sin1 and Sin1β were also found at the plasma membrane and lipid rafts. Both the N-terminal domain and the conserved region in the middle were found to contribute to nuclear localization. Comparative genomic analysis between human, mouse, rat, dog, and chicken Sin1 genes revealed a number of conserved intronic regions, and the putative functions of these were predicted. Additionally, a putative promoter module within a CpG island and encompassing the transcription start site was predicted in all species. The human CpG island was found to have promoter activity in HEK293 cells. Using bioinformatics, genes that may be co-regulated with Sin1 were identified. These genes contained the Sin1 promoter module, and were found to co-express in large scale gene expression studies. Most of these genes were directly involved in the cellular response to pathogen infection, suggesting a conserved role for Sin1 in this pathway. Key biochemical functions of the Sin1 proteins were also identified, including the ability of Sin1 proteins to form dimers, and the ability of over-expressed Sin1 to induce apoptosis (mediated through the conserved region in the middle). Additionally, endogenous Sin1 protein levels were found to change following serum deprivation and hypoosmotic stress. Together, these studies have provided significant insight into the cellular role of Sin1, suggesting a role in inducing apoptosis as part of the IFN response to viral infection. The biological significance of the Sin1 proteins is discussed in the context of their predicted functions and the evolution of the protein family.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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Nilsson, Jonas. "The LRIG-family : identification of novel regulators of ErbB signaling with clinical implications in astrocytoma /". Doctoral thesis, Umeå : Department of Radiation Sciences, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-783.

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Bartee, Eric Carter. "Discovery and characterization of a novel family of human ubiquitin ligases termed Membrane Associated RING-CH (MARCH) proteins". Oregon Health & Science University, 2007. http://content.ohsu.edu/u?/etd,629.

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Ph.D.
Molecular Microbiology and Immunology
Both poxviruses and γ2-herpesviruses share the K3-family of viral immune evasion proteins. These proteins are characterized by an amino-terminal RING-CH domain followed by two transmembrane domains. We analyzed several human homologues of the K3-family termed membrane-associated RING-CH (MARCH) proteins. All MARCH proteins localized to subcellular membranes while several reduced surface levels of known K3-family substrates. Thus, MARCH proteins appear to be structurally and functionally homologous to viral K3 proteins. One of the major challenges in determining the function of this family is the identification of their physiological substrates. To overcome this we created a quantitative proteomics approach which can be used to identify novel substrates for both the K3- and MARCH-families. Using stable isotope labeling by amino acids in cell culture, we compared the proteome of plasma membrane, golgi, and endoplasmic reticulum membranes in the presence and absence of K5 and MARCH-VIII. Quantitative mass spectrometric protein identification from these fractions revealed that CD316 (bone marrow stromal antigen 2), CD166 (activated leukocyte cell adhesion molecule) and syntaxin-4 were consistently underrepresented in the plasma membrane of K5 expressing cells, while CD44, CD81 (TAPA-1) and B-cell receptor-associated protein 31kDa (Bap31) were consistently underrepresented in the plasma membrane of MARCH-VIII expressing cells. Furthermore, downregulation of each of these proteins was independently confirmed. Our results both identify and characterize a novel family of human ubiquitin ligase enzymes and elucidate a novel technique which can analyze this family and be easily adapted to the analysis of other cellular enzymes viral immune modulators.
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Iwai, Akio. "Siah-1L, a novel transcript variant belonging to the human Siah family of proteins, regulates β-catenin activity in a p53-dependent manner". Kyoto University, 2005. http://hdl.handle.net/2433/144711.

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Ruane, Peter Thomas. "Functional characterisation of human EB protein family member EB2". Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.550859.

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Dynamic protein filaments in eukaryotic cells make up cytoskeletal arrays that perform essential functions. Microtubules form part of the cytoskeleton, and impart structure, integrity and organisation to cells. End binding (EB) proteins are an evolutionarily conserved family which associate with the dynamic ends of microtubules, where they act to control microtubule growth and recruit other proteins that localise to this site (+ TIPs). EB2 is one of three vertebrate EB proteins but its role is unclear because it exhibits weak EB protein activity. This thesis describes molecular and cell . biological experiments designed to functionally characterise human EB2. Fourteen human cell lines were all shown to express EB2 at lower levels than EB 1, while isolation of EB2 in HeLa cells by siRNA-mediated knock down of EB 1 and EB3 confirmed reports that EB2 is outcompeted at microtubule ends by EB 1 and EB3. Analysis of individual microtubules corroborated proposals that EB2 has lower affinity for microtubule tips than EB 1, and also suggested that EB proteins interact more strongly with the proximal region of microtubule tips than the distal region. Furthermore, the + TIP CLIP-170 localised to this distal region independently of EB proteins, implicating an activatory rather than direct-coupling role for EB proteins in the recruitment of CLIP-170. Additionally, the functional effects of structural divergences in EB2 were examined by mutation. An N-terminal extension, EB2 Nose, was shown to attenuate + TIP binding through a functional interaction with 322pQ323 in the C- terminal tail of EB2. A putative SxIP motif, 25TIIp28, was identified within EB2 Nose which contributed to this attenuation. It is proposed from these findings that EB2 is autoinhibited for + TIP binding by intramolecular interactions, between EB2 Nose and 322pQ323, and between 25Tllp28 and the C-terminal EB domain. These data portray EB2 as an unproductive EB protein, and a '+ TIP spacer' function is postulated.
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Temprano, López Ana. "The lipin protein family in human adipocytes: lipid metabolism and obesity". Doctoral thesis, Universitat Rovira i Virgili, 2016. http://hdl.handle.net/10803/398025.

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Les lipins són una família conservada evolutivament de fosfatases de fosfatidat (PAP1) dependents de Mg2+, que generen diacilglicerol per a la síntesi de fosfolípids i triacilglicerol. En mamífers, la família consta de lipina-1, lipina-2 i lipina-3. Mentre en ratolins la mutació del gen Lpin1 causa lipodistròfia, les mutacions deletèries en el gen LPIN1 en humans no afecten la distribució del greix. No obstant, persones amb diabetis tipus 2 mostren nivells reduïts de l'expressió de LPIN1 i de l'activitat PAP1. Aquesta tesi estudia el paper de les lipins en el teixit adipós humà, la adipogènesi i la lipòlisi. Descobrim que la expressió de gens i proteïnes lipin és alterada en el teixit adipós de les persones amb diabetis tipus 2. Silenciant cada membre de la família lipin en la línia cel•lular humana de preadipòcits del síndrome Simpson-Golabi-Behmel (SGBS), mostrem que mentre que els tres membres tenen un paper en el primers estadis de l’adipogènesi, els preadipòcits silenciats de lipin es diferencien i acumulen lípids neutres, la qual cosa condueix a la hipòtesi de l'existència de vies alternatives per a la síntesi de triacilglicerol en adipòcits humans quan es reprimeix l'expressió de les lipin. Les lipin participen també en el reciclatge d'àcids grassos alliberats mitjançant la via lipolítica. Després de la inducció de la lipòlisi, les lipines són defosforilades i es desplacen a la membrana del reticle endoplasmàtic, on exerceixen la seva funció enzimàtica. Aquesta activació és induïda pels àcids grassos alliberats i s'inverteix amb la presència d’albúmina o triacsin C. La inducció d’adipòcits silenciats de cada lipina demostra el seu paper en el metabolisme dels lípids neutres. En resum, les lipin semblen no tenir un paper imprescindible en la adipogènesi humana però sí poden comprometre el reciclatge d'àcids grassos, important per a la homeòstasis lipídica.
Las lipinas son una familia de fosfatasas de fosfatidato (PAP1) dependientes de Mg2+ evolutivamente conservadas, que generan diacilglicerol para la síntesis de fosfolípidos y triacilglicerol. En mamíferos, la familia consiste en lipina-1, lipina-2, y lipina-3. Mientras en ratones la mutación del gen Lpin1 causa lipodistrofia, las mutaciones deletéreas en el gen LPIN1 en humanos no afectan a la distribución de grasa. Sin embargo, los individuos con diabetes tipo 2 manifiestan niveles reducidos de expresión de LPIN1 y de actividad PAP1. En esta tesis doctoral se estudia la función de las lipinas en el tejido adiposo humano, la adipogénesis y la lipólisis. Descubrimos que la expresión génica y proteica de las lipinas está alterada en el tejido adiposo de individuos con diabetes tipo 2. La depleción de cada miembro de las lipinas en la línea celular humana de preadipocitos del síndrome Simpson–Golabi–Behmel (SGBS), mostró que, a pesar de que los tres miembros tienen un papel en la adipogénesis temprana, los adipocitos deplecionados de lipinas se diferencian y acumulan lípidos neutros, llevándonos a la hipótesis de la existencia de vías alternativas para la síntesis de triacilglicerol en adipocitos humanos cuando la expresión de las lipinas es reprimida. Las lipinas también intervienen en el reciclaje de los ácidos grasos liberados por la vía lipolítica. Tras la inducción de la lipólisis, las lipinas son defosforiladas y se desplazan a la membrana del retículo endoplásmico, donde ejercen su función. Esta activación es inducida por los ácidos grasos liberados, y revertida con albúmina o triacsin C. La depleción de cada lipina en adipocitos SGBS y posterior inducción de la lipólisis, demuestra su papel en el metabolismo de lípidos neutros. En resumen, las lipinas parecen no tener un papel indispensable en la adipogénesis humana pero sí comprometer el reciclaje de ácidos grasos, importante para la homeostasis lipídica.
Lipins are evolutionarily conserved Mg2+-dependent phosphatidate phosphatases (PAP1) that generate diacylglycerol for phospholipid and triacylglycerol synthesis. In mammals the Lipin family consists of lipin-1, lipin-2 and lipin-3. Whereas mutations in the Lpin1 gene cause lipodystrophy in mouse models, LPIN1 deleterious mutations in humans do not affect fat distribution. However, reduced LPIN1 expression and PAP1 activity have been described in participants with type 2 diabetes. In this doctoral thesis we investigate the roles of all lipin family members in human adipose tissue, adipogenesis and lipolysis. We found that adipose tissue gene and protein expression of the lipin family is altered in type 2 diabetes. Depletion of every lipin family member in a human Simpson–Golabi–Behmel syndrome (SGBS) pre-adipocyte cell line showed that even though all members alter early stages of adipogenesis, lipin-silenced cells differentiate and accumulate neutral lipids, pointing to the hypothesis of alternative pathways for triacylglycerol synthesis under repression of lipin expression. Lipins also have a role in the recycling of the fatty acids released by the lipolytic pathway. They become dephosphorylated upon lipolytic induction, and translocate to their active site, the endoplasmic reticulum membrane. This activation is induced by fatty acids and reversed with albumin or triacsin C. Depletion of every lipin member and subsequently stimulation of lipolysis in SGBS adipocytes revealed a role for lipins in neutral lipid metabolism. Overall, our data support that lipins may not have an indispensable role in adipogenesis, but their depletion compromise fatty acid recycling and lipid homeostasis.
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Chan, Che-man, i 陳志敏. "Functional study of spike protein of a novel human coronavirus HKU1". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41896932.

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Chan, Che-man. "Functional study of spike protein of a novel human coronavirus HKU1". Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41896932.

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Rhyner, Johannes A. "The human calmodulin gene family and characterization of the calmodulin-like protein /". [S.l.] : [s.n.], 1994. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10508.

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Książki na temat "Novel Human Protein Family"

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Sawzdargo, Marek. Discovery of novel G protein-coupled receptor genes including human GALR3 receptor gene. Ottawa: National Library of Canada, 1999.

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The human bobby: A novel. New York, NY: Simon & Schuster, 2010.

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Docherty, John Martin. The cloning and characterization of three novel human genes encoding G protein-coupled receptors. Ottawa: National Library of Canada, 1994.

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Borchert, Monika. Characterization of p34, a human collagen-binding membrane protein in the annexin family. München: H. Gertner, 1990.

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Boleto: A novel. Minneapolis, Minn: Graywolf Press, 2012.

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Castillo, Ana. Guardians: A novel. New York: Random House Trade Paperbacks, 2008.

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The baby trail: A novel. New York: Atria Books, 2005.

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Perfect life: A novel. New York: W.W. Norton & Co., 2009.

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Picoult, Jodi. Sing you home: A novel. New York: Pocket Books, 2014.

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Maitland, Sara. Daughter of Jerusalem: A novel. New York: H. Holt, 1995.

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Części książek na temat "Novel Human Protein Family"

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Hilt, Dana C., i Douglas Kligman. "The S-100 Protein Family: A Biochemical and Functional Overview". W Novel Calcium-Binding Proteins, 65–103. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76150-8_6.

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Satpute, Babasaheb S., i Raghav Yadav. "Recognition of Protein Family Using a Novel Classification System". W Communications in Computer and Information Science, 354–61. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1423-0_37.

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Krishna, Neel K., i Kenji M. Cunnion. "Human Astrovirus Coat Protein: A Novel C1 Inhibitor". W Advances in Experimental Medicine and Biology, 228–42. New York, NY: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-78952-1_17.

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Matsuda, Y., A. Tsuji, H. Nagamume, T. Akamatsu, C. Hine, K. Muramatsu, K. Mori, Y. Tamai i K. Yonemoto. "Novel Members of Mammalian Kexin Family Proteases, Pace 4C, Pace 4D, PC 7A and PC 7B". W Intracellular Protein Catabolism, 63–71. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0335-0_7.

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Longbottom, David, i Veronica van Heyningen. "The Calgranulins, Members of the S-100 Protein Family: Structural Features, Expression, and Possible Function". W Novel Calcium-Binding Proteins, 191–223. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76150-8_12.

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Hwa, Kuo-yuan, Wan-Man Lin, Chueh-Pai Lee i Mei-Yu Chen. "Knowledge Management on the Novel LAGE-Like GlcNAc-Transferase Protein Family". W Bio-Science and Bio-Technology, 141–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-10616-3_19.

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Izzo, P., P. Costanzo, A. Lupo i F. Salvatore. "NOVEL ASPECTS OF THE HUMAN ALDOLASE GENE FAMILY AND ITS EXPRESSION IN TUMOR CELLS". W Human Tumor Markers, redaktorzy F. Cimino, G. D. Birkmayer, J. V. Klavins, E. Pimentel i F. Salvatore, 889–98. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110846515-064.

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Doulami, Christiana, Uday Kishore, Robert B. Sim i Wilhelm Schwaeble. "Mannose-Binding Lectin in Human Health and Disease". W The Collectin Protein Family and Its Multiple Biological Activities, 17–47. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-67048-1_2.

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Bartalena, Luigi, Settimio Grimaldi i Jacob Robbins. "Human Hepatoma (Hep G2) Cells Secrete a Novel T4-Binding Protein (27 K Protein)". W Frontiers in Thyroidology, 477–80. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5260-0_84.

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Gerke, Volker. "p11, A Member of the S-100 Protein Family, is Associated with the Tyrosine Kinase Substrate p36 (Annexin II)". W Novel Calcium-Binding Proteins, 139–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76150-8_9.

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Streszczenia konferencji na temat "Novel Human Protein Family"

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Jovanović-Šanta, Suzana S., Aleksandar M. Oklješa, Antos B. Sachanka, Yaraslau U. Dzichenka i Sergei A. Usanov. "17-SUBSTITUTED STEROIDAL TETRAZOLES – NOVEL LIGANDS FOR HUMAN STEROID-CONVERTING CYP ENZYMES". W 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.336js.

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In animal and human organisms, there are many enzymes, members of the family of heme- containing proteins, cytochromes P450 (CYPs), included in the biosynthesis and metabolism of many biomolecules, as cholesterol, bile acids, sex, and corticosteroid hormones, as well as in metabolism of drugs and xenobiotics. It is also well-known that different imidazole and triazole derivatives are efficient inhibitors of CYPs activity. In this study, we present in vitro screening of binding of novel androstane derivatives with tetrazole- containing substituents in position 17 to human recombinant steroid-converting CYP enzymes: CYP7A1, CYP7B1, CYP17A1, CYP19, and CYP21. Initial screening was performed using a high throughput screening approach, while the affinity of the ligands was analyzed using spectrophotometric titration. For some among tested compounds type I spectral response (substrate-like binding) for CYP7A1 selectively, while for one compound type II spectral response (inhibitor-like binding) for CYP21 were detected, with micromolar values of Kds. Interestingly, one compound with mixed spectral response was found to bind for CYP7B1, which means that there are two optimal positions of the ligand inside the protein active site. Such results could be useful in CYP-inhibiting drug development, during a fast, high-throughput screening of pharmacological potential of novel compounds, as well as in side- effects recognizing.
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Fujikawa, K., T. Funakoshi, R. L. Heimark i J. F. Tait. "HUMAN PLACENTAL ANTICOAGULANT PROTEIN". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642949.

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Endothelium is important to maintain blood fluidity preventing coagulation. Glycosaminoglycan in the endothelial cell plasma membrane has been thought to prevent activation of blood coagulation. Heparin-like compound, which is a potent anticoagulant activity, has been localized on the surface of the cultured endothelial cells. Anticoagulant action associated with thrombomodulin, which is present in endothelial cells, is another mechanism to provide hemostatic nature of endothelial cells.We wondered whether any other intracellular protein(s) is involved in coagulation. We looked for such a protein(s) in cultured bovine aortic endothelial cells. We soon found an anticoagulant activity in the soluble fraction of endothelial cells and it was partially purified. This activity was adsorbed to DEAE-Sepharose and eluted from a gel filtration column in a molecular weight range of 30,000-40,000. However, limited amounts of the cells made it difficult to purify this activity. We then chose human placenta as a substitute source of this protein and have continued the purification of this anticoagulant activity.In this communication, we describe the isolation and characterization of a placental anticoagulant protein, called "PAP", which is silmilar or possible same as the endothelial anticoaguant protein. PAP was purified from the soluble fraction of human placenta by ammonium sulfate precipitation and column chromatography on DEAE-Sepharose, Sephadex G-75, and mono S (Pharmacia). Approximately 20 mg of the protein was purified from one placenta. The purified protein gave a single band by SDS polyacrylamide gel electrophoresis with a molecular weight of 36,500. This protein inhibited both kaolin- and thromboplastin-induced partial thromboplastin times of normal human plasma. It also inhibited the clotting time of platelet-rich plasma induced by factor Xa, but did not affect the thrombin activity of fibrinogen-fibrin conversion. The purified protein completely inhibited the prothrombin activation by reconstituted prothrombinase. The protein neither inhibited the amidolytic activity of factor Xa nor bound factor Xa. This protein specifically bound to phospholipid vesicles (20% phosphatidylserine and 80% phosphatidylcholine) in the presence of calcium ions. These results indicate that PAP inhibits coagulation through the binding to phospholipid vesicles. The study on the amino acid sequence of PAP is in progress in our laboratory. Surprisingly, the sequence analysis of the cyanogen bromide fragments revealed that PAP is a new member of the lipocortin or calpactin family. The sequences of several cyanogen bromide fragments of PAP aligns with the sequences of lipocortin I and II with over 50% identity.Since PAP interacts directly with phospholipid rather than factor Xa, other activation steps in the coagulation cascade, in which phospholipid is involved, are pro^|bly affected by PAP. These reactions are the activation of factor X by a complex of factor IXa-factor VIIIa-phospholipid-Ca++ and the activations of factor X and factor IX by a tissue factor-factor VIIa-Ca++ complex.Reutelingsperger et. al,, have reported the isolation of a novel inhibitor from arteries of human umbilical cord. This protein inhibited the prothrombin activation by prothrombinase. The authors proposed that the inhibition mechanism of this inhibitor was a competition with factor Xa for binding to phospholipid. This protein is very similar to PAP as to the mode of inhibition. The molecular weight of this inhibitor is 32,000, which is slightly smaller than PAP. With the limited chemical characterization of this protein, presently it is difficult to identify this inhibitor with PAP.At the present time, the physiological role and origin of PAP is not known. PAP may originate from the endothelium of placenta, because we have detected a PAP-like anticoagulant activity in bovine aortic endothelial cells. This activity and PAP were quite alike in the purification up to the gel filtration step. If PAP antibody recognizes the antigen in the endothelial cells, it is interesting to see whether PAP localizes on the surface or inside the cells. Nevertheless, if PAP is present in the endothelial cells, it may play an important role to maintain the hemostatic nature of endothelium. PAP may bind phospholipid components at injured sites, before coagulation factors come in contact with lipid components and initiate thrombolytic events.
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Tokunaga, F., T. Miyata, T. Nakamura, T. Morita i S. Iwanaga. "LIPOPOLYSACCHARIDE-SENSITIVE SERINE-PROTEASE ZYMOGEN (FACTOR C) OF LIMULUS HEMOCYTES: IDENTIFICATION AND ALIGNMENT OF PROTEOLYTIC FRAGMENTS PRODUCED DURING THE ACTIVATION SHOW THAT IT IS A NOVEL TYPE OF SERINE-PROTEASE". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644609.

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Limulus clotting factor, factor C, is a lipopolysaccharide (LPS)-sensitive serine-protease zymogen present in the hemocytes. It is a two-chain glycoprotein (M.W. = 123,000) composed of a heavy chain (M.W. = 80,000) and a light chain (M.W. = 43,000) T. Nakamura et al. (1986) Eur. J. Biochem. 154, 511-521 .On further studies of this zymogen, a single-chain factor C (M.W. = 123,000) was identified by Western blotting technique. The heavy chain had an NH2-terminal sequence of Ser-Gly-Val-Asp-, which was consistent with the NH2-terminal sequence of the single-chain factor C, indicating that the heavy chain is located in the NH2-terminal part of the zymogen. The light chain had an NH22-terminal sequence of Ser-Ser-Gln-Pro-. Incubation of the two-chain zymogen with LPS resulted in the cleavage of a Phe-Ile bond between residues 72 and 73 of the light chain. Concomitant with this cleavage, the A (72.amino acids) and B chains derived from the light chain was formed. The complete amino acid sequence of the A chain was determined by automated Edman degradation. The A chain contained a typical segment which is similar structuraly to those a family of repeats in human β2 -glycoprotein I, complement factors B, Clr, Cls, H, C4b-binding protein, 02, coagulation factor XIII b subunit, haptoglobin a chain, and interleukin 2 receptor. The NH2-terminal sequence of the B chain was Ile-Trp-Asn-Gly-. This chain contained the serine-active site sequence of -ASP-Ala-Cys-Ser-Gly-Asp-SER-Gly-Gly-Pro-.These results indicate that limulus factor C exists in the hemocytes in a single-chain zymogen form and is converted to an active serine-protease by hydrolysis of a specific Phe-Ile peptide bond. The correlation of limulus factor C and mammalian complement proteins was also suggested.
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Wasi, S., P. Alles, D. Gauthier, U. Bhargava, J. Farsi, J. E. Aubin i J. Sodeki. "STUDIES ON SMALL MOLECULAR WEIGHT ADHESION PROTEINS (SAPs) FROM CONNECTIVE TISSUES". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643556.

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We have identified a family of low molecular weight proteins with cell attachment properties in a variety of soft and mineralised connective tissues (Wong et al., Biochem. J. 232, 119, 1985). For further characterisation of these proteins we extracted porcine bones with 4 M guanidine hydrochloride and purified the proteins on a series of gel filtration columns The purifed SAPs comprise three bands with Mr -14 000 -17 000. All three proteins bound to heparin-sepahrose in both the presence and absence of 4M urea, and when eluted with 2 M NaCl they retained their cell binding capacity. These proteins promoted the adhesion and spreading of a variety of cell types, including normal fibroblasts, osteoblasts, and epithelial cells, and tumour (osteosarcoma) cells. On Western blotting SAPs did not cross-react with antibodies against fibronectin, laminin or type I collagen; however, they were recognised by a monoclonal antibody to human vitronectin, a polyclonal antibody to bovine vitronectin and polyclonal antibody to human somatomedin B. Dose response experiments indicated that maximum attachment of human gingival fibroblasts occurred in the presence or absence of fetal bovine serum on wells precoated with 2.5 μg/cm2 of SAPs. Attachment of cells to these proteins was partially inhibited by the synthetic pentapeptide Gly-Arg-Gly-Asp-Ser. Utilising the nitrocellulose cell binding assay of Hayman et al (J. Cell. Biol. 95, 20, 1982), the cell attachment to these proteins could be completely inhibited by heparin (100 units/mL) whereas up to 1000 units/mL of heparin had no inhibitory effect on cell attachment to fibronectin and vitronectin. The occurrence of these proteins in a variety of connective tissues and their recognition by different cell types may reflect their general biological role in adhesive mechanisms in both hard and soft connective tissues. Currently, we are investigating the relationship between SAPs and vitronectin, since it is possible that SAPs represent a tissue-processed form of vitronectin or may be novel attachment proteins with regions of homology with vitronectin
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Maheshwari, Reeti, Melissa Schluter, Danielle Pepin i Joseph Hwang. "Abstract 4319: Analysis of Bcl-2 family members and protein-protein interactions using novel multiplex immunoassays". W Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4319.

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Gu, Hong, i Junzhe Cao. "A novel integrated method for human multiplex protein subcellular localization prediction". W 2013 IEEE International Conference on Big Data. IEEE, 2013. http://dx.doi.org/10.1109/bigdata.2013.6691734.

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Yazdani, Mehrdad, Bryn C. Taylor, Justine W. Debelius, Weizhong Li, Rob Knight i Larry Smarr. "Using machine learning to identify major shifts in human gut microbiome protein family abundance in disease". W 2016 IEEE International Conference on Big Data (Big Data). IEEE, 2016. http://dx.doi.org/10.1109/bigdata.2016.7840731.

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Seaman, Marc E., i Kimberly A. Kelly. "Abstract 3891: Hornerin: a novel, non-VEGF mediated human tumor angiogenic protein." W Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3891.

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Wang, Jing, Xuezhi Bi i Shang Li. "Abstract 3469: Identification of novel human telomerase associated protein by mass spectrometry". W Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3469.

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Dejana, E., F. Breviario, F. Bussolino, L. Mussoni i A. Mantovani. "PLEIOTROPIC EFFECT OF INTERLEUKIN-1 ON ENDOTHELIAL CELLS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643984.

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Inflammatory processes are often associated with pathological alteration of the vessel wall and sometimes with local or disseminated thrombotic phenomena. Interleukin-1 (IL-1), a monokine produced by activated cells of the monocyte/macrophage lineage and responsible of most of the changes associated with the inflammatory acute phase response, appears to dramatically' modify several endothelial cell (EC) functions. Some groups including ours (for review 1) have shown that IL-1 stimulates prostacyclin (PGI2), platelet activating factor (PAF), plasminogen activator inhibitor (PAi), thromboplastin (PCA) synthesis by cultured human EC in vitro. In addition IL-1 can act directly on EC to increase neuthophil and other leukocyte adhesion on their surface (2). All these effects, in contrast to previously described inducers, require a long time of interaction (30 min to 4 hours) of IL-1 with EC to be apparent and then last for several hours (4 to 12 hours). The IL-1 effects are concentration dependent (minimal active concentration being about 1 unit/ml) and require protein and RNA synthesis. To better define the structural requirement for IL-1 induced modification of EC functions we compared the activity of different IL-1 molecular species. Our approach is based on the observation that IL-1 is indeed a family of polypeptides biochemically different(3). At least two dissimilar gene products have been cloned with very limited homology (denominated α and β). These molecules, though biochemically different, share common activities and possibly the same receptor in different cell types. On EC we investigated whether the αand β IL-1 forms have similar biological activities (4). All the IL-1 preparations used were active on thymocyte costimulatory assay and comparison was made on the basis of the concentrations of these agents equally active on this assay.Human recombinant IL- αandβ (hr IL-1 α and hr IL-1 β) were both active in stimulating PGI2, PCA, PAi production and in increasing neutrophil adhesion to EC. In contrast PAF synthesis was Stimulated by hr IL-1 α but not by hr IL-1 β. Murine recombinant IL-1 (mr IL-1 α highly homologous with hr IL-1 < α, at concentrations able to maximally activate thymocytes was inactive on PGI2, PCA and in increasing neutrophil adhesion to EC. In contrast, mr IL-1 α was equally effective on PAF production as hr IL-1 α. A short peptide fragment of hr IL-1β (fragment 167-171) was synthesized on the basis of its predicted exposure on the surface of the molecule (5). This peptide is also located in a region (150-186) of high homology between hr IL-1α and β sequences. While the peptide showed high thymocyte activation capacity it was inactive on EC activities. Overall these results indicate that the α and β forms of human IL-1 elicit largely but not completely overlapping patterns of response in EC. In addition they suggest that the structural requirement for activation by IL-1 is not identical for thymocytes and EC. These results might provide some clues to novel strategies for modulation of IL-1 vascular and immunological activities.1. Mantovani A. and E. Dejana (1987) Biochem. Pharm. 36:301.2. Bevilacqua M. et al. (1985) J. Clin. Invest. 76:20033. Dinarello C.A. (1985) J. Clin. Immunol. 5:287.4. Dejana E. et al. (1987) Blood 69:695.5. Antoni G. et al. (1987) J. Immunol, (in press).
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Raporty organizacyjne na temat "Novel Human Protein Family"

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Manning, Michael. Engineering a Cytolytic Human Protein into a Novel Prostate Cancer Protoxin. Fort Belvoir, VA: Defense Technical Information Center, marzec 2011. http://dx.doi.org/10.21236/ada600512.

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Manning, Michael L. Engineering a Cytolytic Human Protein Into a Novel Prostate Cancer Protoxin. Fort Belvoir, VA: Defense Technical Information Center, marzec 2010. http://dx.doi.org/10.21236/ada603042.

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Richards, Talmesha. Polyamine Analogues as Novel Anti-HER Family Agents in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2008. http://dx.doi.org/10.21236/ada513832.

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Richards, Talmesha. Polyamine Analogues as Novel Anti-HER Family Agents in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2007. http://dx.doi.org/10.21236/ada477006.

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Barakat, Dr Shima, Dr Samuel Short, Dr Bernhard Strauss i Dr Pantea Lotfian. https://www.food.gov.uk/research/research-projects/alternative-proteins-for-human-consumption. Food Standards Agency, czerwiec 2022. http://dx.doi.org/10.46756/sci.fsa.wdu243.

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The UK is seeing growing interest in alternative protein sources to traditional animal-based proteins such as beef, lamb, pork, poultry, fish, eggs, and dairy. There is already an extensive market in alternative protein materials, however, technological advances combined with the pressure for more sustainable sources of protein has led to an acceleration of innovation and product development and the introduction of a large amount of new alternative protein ingredients and products to the market. These have the potential to dramatically impact on the UK food system. This report is a combination of desk research, based on thorough review of the academic and non-academic literature and of the alternative proteins start-up scene, and presents an analysis of the emerging market for alternative proteins, the potential implications and the potential policy responses that the FSA might need to consider. Four main categories of alternative proteins are presented and reviewed in this report: Plant-based meat substitutes Novel protein sources Proteins and biomass biosynthesised by microorganisms Cultured meat
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Heitman, Joseph. Novel Gbeta Mimic Kelch Proteins (Gpb1 and Gpb2 Connect G-Protein Signaling to Ras via Yeast Neurofibromin Homologs Ira1 and Ira2: A Model for Human NF1. Fort Belvoir, VA: Defense Technical Information Center, marzec 2008. http://dx.doi.org/10.21236/ada483900.

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Heitman, Joseph, i Toshiaki Harashima. Novel Gbeta Mimic Kelch Proteins (Gpb1 and Gpb2 Connect G-Protein Signaling to Ras via Yeast Neurofibromin Homologs Ira1 and Ira2. A Model for Human NF1. Fort Belvoir, VA: Defense Technical Information Center, marzec 2007. http://dx.doi.org/10.21236/ada479028.

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Heitman, Joseph, i Toshiaki Harashima. Novel Gbeta Mimic Kelch Proteins Gpb1 and Gpb2 Connect G-Protein Signaling to Ras Via Yeast Neurofibromin Homologs Ira 1 and Ira 2: A Model for Human NF1. Fort Belvoir, VA: Defense Technical Information Center, marzec 2005. http://dx.doi.org/10.21236/ada446943.

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Heitman, Joseph. Novel Gbeta Mimic Kelch Proteins Gpb1 and Gpb2 Connect G-Protein Signaling to Ras via Yeast Neurofibromin Homologs Ira 1 and Ira 2: A Model for Human NF1. Fort Belvoir, VA: Defense Technical Information Center, marzec 2006. http://dx.doi.org/10.21236/ada469875.

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Dolja, Valerian V., Amit Gal-On i Victor Gaba. Suppression of Potyvirus Infection by a Closterovirus Protein. United States Department of Agriculture, marzec 2002. http://dx.doi.org/10.32747/2002.7580682.bard.

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The plant virus family Polyviridae is the largest and most destructive of all plant viruses. Despite the continuous effort to develop resistant plant varieties, there is a desperate need for novel approaches conferring wide-range potyvirus resistance. Based on experiments with the tobacco etch potyvirus (TEV)-derived gene expression vector, we suggested approach for screening of the candidate resistance genes. This approach relies on insertion of the genes into a virus vector and evaluation of the phenotypes of the resulting recombinant viruses. The genes which suppress infection by the recombinant virus are selected as candidates for engineering transgenic resistance. Our analysis of the TEV variants expressing proteins of the beet yellows closterovirus (BYV) revealed that one of those, the leader proteinase (L-Pro), strongly and specifically interfered with the hybrid TEV infection. Since closterovirus L-Pro is evolutionary related to potyviral helper component-proteinase (HC-Pro), we suggested that the L-Pro interfered with HC-Pro function via a trans-dominant inhibitory effect. Based on these findings, we proposed to test two major hypotheses. First, we suggested that L-Pro-mediated suppression of potyvirus infection is a general phenomenon effective against a range of potyviruses. The second hypothesis stated that the suppression effect can be reproduced in transgenic plants expressing L-Pro, and can be utilized for generation of resistance to potyviruses. In accord with these hypotheses, we developed two original objectives of our proposal: A) to determine the range of the closterovirus-derived suppression of potyviral infection, and B) to try and utilize the L-Pro-mediated suppression for the development of transgenic resistance to potyviruses. In the first phase of the project, we have developed all major tools and technologies required for successful completion of the proposed research. These included TEV and ZYMV vectors engineered to express several closteroviral L-Pro variants, and generation of the large collection of transgenic plants. To our satisfaction, characterization of the infection phenotypes exhibited by chimeric TEV and ZYMV variants confirmed our first hypothesis. For instance, similar to TEV-L- Pro(BYV) chimera, ZYMV-L-Pro(LIYV) chimera was debilitated in its systemic spread. In contrast, ZYMV-GUS chimera (positive control) was competent in establishing vigorous systemic infection. These and other results with chimeric viruses indicated that several closteroviral proteinases inhibit long-distance movement of the potyviruses upon co-expression in infected plants. In order to complete the second objective, we have generated ~90 tobacco lines transformed with closteroviral L-Pro variants, as well as ~100 lines transformed with BYV Hsp70-homolog (Hsp70h; a negative control). The presence and expression of the trans gene in each line was initially confirmed using RT-PCR and RNA preparations isolated from plants. However, since detection of the trans gene-specific RNA can not guarantee production of the corresponding protein, we have also generated L-Pro- and Hsp70h-specific antisera using corresponding synthetic peptides. These antisera allowed us to confirm that the transgenic plant lines produced detectable, although highly variable levels of the closterovirus antigens. In a final phase of the project, we tested susceptibility of the transgenic lines to TEV infection. To this end, we determined that the minimal dilution of the TEV inoculum that is still capable of infecting 100% of nontransgenic plants was 1:20, and used 10 plants per line (in total, ~2,000 plants). Unfortunately, none of the lines exhibited statistically significant reduction in susceptibility. Although discouraging, this outcome prompted us to expand our experimental plan and conduct additional experiments. Our aim was to test if closteroviral proteinases are capable of functioning in trans. We have developed agroinfection protocol for BYV, and tested if co- expression of the L-Pro is capable of rescuing corresponding null-mutant. The clear-cut, negative results of these experiments demonstrated that L-Pro acts only in cis, thus explaining the lack of resistance in our transgenic plants. We have also characterized a collection of the L-Pro alanine- scanning mutants and found direct genetic evidence of the requirement for L-Pro in virus systemic spread. To conclude, our research supported by BARD confirmed one but not another of our original hypotheses. Moreover, it provided an important insight into functional specialization of the viral proteinases and generated set of tools and data with which we will be able to address the molecular mechanisms by which these proteins provide a variety of critical functions during virus life cycle.
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