Molecular cloning and phenotypic analysis of drug-resistance mutants with relevant S-region variants of HBV for a patient during 189-month anti-HBV treatment

2019 ◽  
Vol 24 (4) ◽  
pp. 237-246 ◽  
Author(s):  
Yan Liu ◽  
Chunchen Wu ◽  
Rongjuan Chen ◽  
Xiaodong Li ◽  
Zhihui Xu ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Molecular Cloning ◽  
Phenotypic Analysis ◽  
Resistance Mutants

scholarly journals A Novel Five-Transmembrane Hematopoietic Stem Cell Antigen: Isolation, Characterization, and Molecular Cloning

Blood ◽  
1997 ◽  
Vol 90 (12) ◽  
pp. 5013-5021 ◽  
Author(s):  
Sheri Miraglia ◽  
Wayne Godfrey ◽  
Amy H. Yin ◽  
Kristin Atkins ◽  
Roger Warnke ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Surface ◽  
Molecular Cloning ◽  
Surface Antigen ◽  
Fetal Liver ◽  
Cell Surface Antigen ◽  
Northern Analysis ◽  
Phenotypic Analysis ◽  
Hematopoietic Stem ◽  
C Terminus

Phenotypic analysis of hematopoietic stem and progenitor cells (HSCs) has been an invaluable tool in defining the biology of stem cell populations. We have recently described the production of AC133, a monoclonal antibody (MoAb) that binds to a novel cell surface antigen present on a CD34bright subset of human HSCs. This antigen is a glycosylated protein with a molecular weight of 120 kD. Here, we report the molecular cloning of a cDNA encoding this antigen and show that it does not share homology with any previously described hematopoietic or other cell surface antigen(s). The AC133 polypeptide has a predicted size of 97 kD and contains five-transmembrane (5-TM) domains with an extracellular N-terminus and a cytoplasmic C-terminus. Whereas the expression of tetraspan (4-TM) and 7-TM molecules is well documented on mature and immature hematopoietic cells and leukocytes, this 5-TM type of structure containing two large (255–amino acid [aa] and 290-aa) extracellular loops is unique and does not share sequence homology with any known multi-TM family members. Expression of this protein appears limited to bone marrow in normal tissue by immunohistochemical staining; however, Northern analysis suggests that the mRNA transcript is present in a variety of tissues such as the kidney, pancreas, placenta, and fetal liver. The AC133 antigen is also expressed on subsets of CD34+ leukemias, suggesting that it may be an important early marker for HSCs, as well as the first described member of a new class of TM receptors.

scholarly journals A Novel Five-Transmembrane Hematopoietic Stem Cell Antigen: Isolation, Characterization, and Molecular Cloning

Blood ◽  
1997 ◽  
Vol 90 (12) ◽  
pp. 5013-5021 ◽  
Author(s):  
Sheri Miraglia ◽  
Wayne Godfrey ◽  
Amy H. Yin ◽  
Kristin Atkins ◽  
Roger Warnke ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Surface ◽  
Molecular Cloning ◽  
Surface Antigen ◽  
Fetal Liver ◽  
Cell Surface Antigen ◽  
Northern Analysis ◽  
Phenotypic Analysis ◽  
Hematopoietic Stem ◽  
C Terminus

Abstract Phenotypic analysis of hematopoietic stem and progenitor cells (HSCs) has been an invaluable tool in defining the biology of stem cell populations. We have recently described the production of AC133, a monoclonal antibody (MoAb) that binds to a novel cell surface antigen present on a CD34bright subset of human HSCs. This antigen is a glycosylated protein with a molecular weight of 120 kD. Here, we report the molecular cloning of a cDNA encoding this antigen and show that it does not share homology with any previously described hematopoietic or other cell surface antigen(s). The AC133 polypeptide has a predicted size of 97 kD and contains five-transmembrane (5-TM) domains with an extracellular N-terminus and a cytoplasmic C-terminus. Whereas the expression of tetraspan (4-TM) and 7-TM molecules is well documented on mature and immature hematopoietic cells and leukocytes, this 5-TM type of structure containing two large (255–amino acid [aa] and 290-aa) extracellular loops is unique and does not share sequence homology with any known multi-TM family members. Expression of this protein appears limited to bone marrow in normal tissue by immunohistochemical staining; however, Northern analysis suggests that the mRNA transcript is present in a variety of tissues such as the kidney, pancreas, placenta, and fetal liver. The AC133 antigen is also expressed on subsets of CD34+ leukemias, suggesting that it may be an important early marker for HSCs, as well as the first described member of a new class of TM receptors.

scholarly journals The continuous morbidostat: A chemostat with controlled drug application to select for drug resistance mutants

2020 ◽  
Vol 19 (1) ◽  
pp. 203-220
Author(s):  
Zhenzhen Chen ◽  
◽  
Sze-Bi Hsu ◽  
Ya-Tang Yang ◽  
◽  
...  
Keyword(s):  
Drug Resistance ◽  
Drug Application ◽  
Resistance Mutants

scholarly journals Structural studies of inhibitor complexes of HIV-1 protease and of its drug resistance mutants

1996 ◽  
Vol 52 (a1) ◽  
pp. C201-C202
Author(s):  
T. N. Bhat ◽  
R. S. Randad ◽  
A. Y. Lee ◽  
L. Lubkowska ◽  
S. Munshi ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Structural Studies ◽  
Hiv 1 ◽  
Resistance Mutants

scholarly journals Antiviral Drug Resistance of Human Cytomegalovirus

2010 ◽  
Vol 23 (4) ◽  
pp. 689-712 ◽  
Author(s):  
Nell S. Lurain ◽  
Sunwen Chou
Keyword(s):  
Drug Resistance ◽  
Dna Polymerase ◽  
Human Cytomegalovirus ◽  
Treatment Options ◽  
Antiviral Drug ◽  
Resistance Mutations ◽  
Phenotypic Analysis ◽  
Antiviral Drug Resistance ◽  
Phenotypic Methods ◽  
Approved Drugs

SUMMARY The study of human cytomegalovirus (HCMV) antiviral drug resistance has enhanced knowledge of the virological targets and the mechanisms of antiviral activity. The currently approved drugs, ganciclovir (GCV), foscarnet (FOS), and cidofovir (CDV), target the viral DNA polymerase. GCV anabolism also requires phosphorylation by the virus-encoded UL97 kinase. GCV resistance mutations have been identified in both genes, while FOS and CDV mutations occur only in the DNA polymerase gene. Confirmation of resistance mutations requires phenotypic analysis; however, phenotypic assays are too time-consuming for diagnostic purposes. Genotypic assays based on sequencing provide more rapid results but are dependent on prior validation by phenotypic methods. Reports from many laboratories have produced an evolving list of confirmed resistance mutations, although differences in interpretation have led to some confusion. Recombinant phenotyping methods performed in a few research laboratories have resolved some of the conflicting results. Treatment options for drug-resistant HCMV infections are complex and have not been subjected to controlled clinical trials, although consensus guidelines have been proposed. This review summarizes the virological and clinical data pertaining to HCMV antiviral drug resistance.

scholarly journals Suppressors of yeast actin mutations.

Genetics ◽  
1989 ◽  
Vol 121 (4) ◽  
pp. 659-674 ◽  
Author(s):  
P Novick ◽  
B C Osmond ◽  
D Botstein
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Surface ◽  
Actin Cytoskeleton ◽  
Molecular Cloning ◽  
Temperature Sensitive ◽  
Actin Gene ◽  
Phenotypic Analysis ◽  
Allele Specific ◽  
Cold Sensitive ◽  
Growth Phenotype

Abstract Suppressors of a temperature-sensitive mutation (act1-1) in the single actin gene of Saccharomyces cerevisiae were selected that had simultaneously acquired a cold-sensitive growth phenotype. Five genes, called SAC (suppressor of actin) were defined by complementation tests; both suppression and cold-sensitive phenotypes were recessive. Three of the genes (SAC1, SAC2 and SAC3) were subjected to extensive genetic and phenotypic analysis, including molecular cloning. Suppression was found to be allele-specific with respect to actin alleles. The sac mutants, even in ACT1+ genetic backgrounds, displayed phenotypes similar to those of actin mutants, notably aberrant organization of intracellular actin and deposition of chitin at the cell surface. These results are interpreted as being consistent with the idea that the SAC genes encode proteins that interact with actin, presumably as components or controllers of the assembly or stability of the yeast actin cytoskeleton. Two unexpected properties of the SAC1 gene were noted. Disruptions of the gene indicated that its function is essential only at temperatures below about 17 degrees and all sac1 alleles are inviable when combined with act1-2. These properties are interpreted in the context of the evolution of the actin cytoskeleton of yeast.

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