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40 results on '"Chen, Luojing"'

8. Collectrin (Tmem27) deficiency in proximal tubules causes hypertension in mice and a TMEM27 variant associates with blood pressure in males in a Latino cohort

Author

Chu, Pei-Lun, primary, Gigliotti, Joseph C., additional, Cechova, Sylvia, additional, Bodonyi-Kovacs, Gabor, additional, Wang, Yves T., additional, Chen, Luojing, additional, Wassertheil-Smoller, Sylvia, additional, Cai, Jianwen, additional, Isakson, Brant E., additional, Franceschini, Nora, additional, and Le, Thu H., additional

Published
2023
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15. Kidney stone formation and the gut microbiome are altered by antibiotics in genetic hypercalciuric stone-forming rats

Author

Stern, Joshua M., primary, Burk, Robert D., additional, Asplin, John, additional, Krieger, Nancy S., additional, Suadicani, Sylvia O., additional, Wang, Yi, additional, Usyk, Mykhaylo, additional, Lee, Justin A., additional, Chen, Luojing, additional, Becker, Jennifer, additional, Chan, Michaela, additional, and Bushinsky, David A., additional

Published
2020
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26. Inhibition of COP9-signalosome (CSN) deneddylating activity and tumor growth of diffuse large B-cell lymphomas by doxycycline

Author

Pulvino, Mary, primary, Chen, Luojing, additional, Oleksyn, David, additional, Li, Jing, additional, Compitello, George, additional, Rossi, Randy, additional, Spence, Stephen, additional, Balakrishnan, Vijaya, additional, Jordan, Craig, additional, Poligone, Brian, additional, Casulo, Carla, additional, Burack, Richard, additional, Shapiro, Joel L., additional, Bernstein, Steven, additional, Friedberg, Jonathan W., additional, Deshaies, Raymond J., additional, Land, Hartmut, additional, and Zhao, Jiyong, additional

Published
2015
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31. Adsorption to starch of a beta-galactosidase fusion protein containing the starch-binding region of Aspergillus glucoamylase

Author

Zivko L. Nikolov, Clark Ford, and Chen Luojing

Subjects
Starch, Recombinant Fusion Proteins, Molecular Sequence Data, Restriction Mapping, Biology, Chromatography, Affinity, chemistry.chemical_compound, Affinity chromatography, Genetics, Escherichia coli, Centrifugation, Amino Acid Sequence, Cloning, Molecular, chemistry.chemical_classification, Binding Sites, Base Sequence, food and beverages, General Medicine, Protein engineering, beta-Galactosidase, Fusion protein, Amino acid, Kinetics, Enzyme, Aspergillus, chemistry, Biochemistry, Adsorption, Glucan 1,4-alpha-Glucosidase, Starch binding, Plasmids
Abstract

We have constructed and purified by affinity chromatography three β-galactosidase (βGal) fusion proteins (BSB133, BSBCD8, and BGA 134) containing amino acid (aa) sequences from Aspergillus glucoamylase (GA). BSB 133, containing the C-terminal 133 aa of GA (aa 484–616), adhered to native starch granules with a much higher affinity (Kad = 18 ml/g starch) than a βGal control (Kad = 0.9 ml/g starch). Two other fusion proteins, BSBCD8 and BGA134, similar in size to BSB133, adhered to starch with a relatively low affinity (Kad = 7 ml/g starch, and Kad = 4 ml/g starch, respectively). B SBCD8 differs from BSB 133 by a truncation of 8 aa at the C terminus. BGA134 contains 134 aafrom an overlapping region of GA (aa 380–513). These results confirm the presence of a strong starch-binding region (SBR) included in the C-terminal 133 aa of GA and indicate that the SBR can confer starch-binding activity on a fusion protein produced in Escherichia coli. In the presence of crude soluble cell extracts, the fusion proteins adsorbed by native starch granules with an affinity similar to that of the purified enzymes. BSB133 that had been adsorbed by starch from crude extracts could be eluted at a high level of purity, similar to that achieved by affinity chromatography. These results suggest that it may be feasible to use native starch as an adsorbent for the recovery and purification of recombinant fusion proteins containing the SBR. Starch has many favorable qualities for this application: it is inexpensive, stable, nontoxic, and easy to recover by centrifugation.

Published
1991

38. Collectrin (Tmem27) Deficiency in Proximal Tubule Causes Hypertension in Mice and a TMEM27 Variant Associates with Blood Pressure in Males in a Latino Cohort

Author

Chu, Pei-Lun, Gigliotti, Joseph C., Cechova, Sylvia, Bodonyi-Kovacs, Gabor, Wang, Yves T., Chen, Luojing, Wassertheil-Smoller, Sylvia, Cai, Jianwen, Isakson, Brant E., Franceschini, Nora, and Le, Thu H.

Abstract

Background: Collectrin (Tmem27), an ACE2 homologue, is a chaperone of amino acid transporters in the kidney and endothelium. Global collectrin knockout (KO) mice have hypertension, endothelial dysfunction, exaggerated salt sensitivity, and diminished renal blood flow. This phenotype is associated with altered nitric oxide and superoxide balance, and increased proximal tubule NHE3 expression. Collectrin is located on the X chromosome where genome wide association population studies have largely been excluded. Methods: We generated proximal tubule specific collectrin KO (PT KO) mice to determine the precise contribution of proximal tubule collectrin in blood pressure homeostasis. We also examined the association of human TMEM27 single nucleotide polymorphisms (SNPs) with blood pressure traits in 11,926 HCHS/SOL Hispanic/Latino participants, Results: PT KO mice exhibited hypertension, and this was associated with increased baseline NHE3 expression and diminished lithium excretion. However, PT KO mice did not display exaggerated salt sensitivity nor reduction in renal blood flow, compared to control mice. Furthermore, PT KO mice exhibited enhanced endothelium-mediated dilation, suggesting a compensatory response to systemic hypertension induced by deficiency of collectrin in the PT. In HCHS/SOL participants, we observed sex-specific SNP associations with diastolic blood pressure. Conclusion: Loss of collectrin in the PT is sufficient to induce hypertension, at least in part, through activation of NHE3. Importantly, our model supports the notion that altered renal blood flow may be a determining factor for salt sensitivity. Further studies are needed to investigate the role of the TMEM27 locus on BP and salt-sensitivity in humans.

Published
2022
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39. Collectrin ( Tmem27) deficiency in proximal tubules causes hypertension in mice and a TMEM27 variant associates with blood pressure in males in a Latino cohort.

Author

Chu PL, Gigliotti JC, Cechova S, Bodonyi-Kovacs G, Wang YT, Chen L, Wassertheil-Smoller S, Cai J, Isakson BE, Franceschini N, and Le TH

Subjects
Animals, Female, Humans, Male, Mice, Genome-Wide Association Study, Hispanic or Latino genetics, Mice, Knockout, Sodium Chloride, Dietary metabolism, Sodium-Hydrogen Exchanger 3 genetics, Sodium-Hydrogen Exchanger 3 metabolism, Blood Pressure physiology, Hypertension genetics, Kidney Tubules, Proximal metabolism, Membrane Glycoproteins deficiency, Membrane Glycoproteins genetics
Abstract

Collectrin ( Tmem27 ), an angiotensin-converting enzyme 2 homologue, is a chaperone of amino acid transporters in the kidney and endothelium. Global collectrin knockout (KO) mice have hypertension, endothelial dysfunction, exaggerated salt sensitivity, and diminished renal blood flow. This phenotype is associated with altered nitric oxide and superoxide balance and increased proximal tubule (PT) Na + /H + exchanger isoform 3 (NHE3) expression. Collectrin is located on the X chromosome where genome-wide association population studies have largely been excluded. In the present study, we generated PT-specific collectrin KO (PT KO) mice to determine the precise contribution of PT collectrin in blood pressure homeostasis. We also examined the association of human TMEM27 single-nucleotide polymorphisms with blood pressure traits in 11,926 Hispanic Community Health Study/Study of Latinos (HCHS/SOL) Hispanic/Latino participants. PT KO mice exhibited hypertension, and this was associated with increased baseline NHE3 expression and diminished lithium excretion. However, PT KO mice did not display exaggerated salt sensitivity or a reduction in renal blood flow compared with control mice. Furthermore, PT KO mice exhibited enhanced endothelium-mediated dilation, suggesting a compensatory response to systemic hypertension induced by deficiency of collectrin in the PT. In HCHS/SOL participants, we observed sex-specific single-nucleotide polymorphism associations with diastolic blood pressure. In conclusion, loss of collectrin in the PT is sufficient to induce hypertension, at least in part, through activation of NHE3. Importantly, our model supports the notion that altered renal blood flow may be a determining factor for salt sensitivity. Further studies are needed to investigate the role of the TMEM27 locus on blood pressure and salt sensitivity in humans. NEW & NOTEWORTHY The findings of our study are significant in several ways: 1 ) loss of an amino acid chaperone in the proximal tubule is sufficient to cause hypertension, 2 ) the results in global and proximal tubule-specific collectrin knockout mice support the notion that vascular dysfunction is required for salt sensitivity or that impaired renal tubule function causes hypertension but is not sufficient to cause salt sensitivity, and 3 ) our study is the first to implicate a role of collectrin in human hypertension.

Published
2023
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40. A catalytically inactive form of protein kinase C-associated kinase/receptor interacting protein 4, a protein kinase C beta-associated kinase that mediates NF-kappa B activation, interferes with early B cell development.

Author

Cariappa A, Chen L, Haider K, Tang M, Nebelitskiy E, Moran ST, and Pillai S

Subjects
Animals, Ankyrin Repeat genetics, Ankyrin Repeat immunology, B-Lymphocytes pathology, Bone Marrow Cells cytology, Bone Marrow Cells enzymology, Catalysis, Cell Differentiation genetics, Cell Differentiation immunology, Cell Division genetics, Cell Division immunology, Enzyme Activation genetics, Enzyme Activation immunology, Growth Inhibitors genetics, Growth Inhibitors metabolism, Hematopoietic Stem Cells cytology, Hematopoietic Stem Cells enzymology, Isoenzymes biosynthesis, Isoenzymes genetics, Isoenzymes metabolism, Isoenzymes physiology, Lymphocyte Activation genetics, Lymphopenia enzymology, Lymphopenia immunology, Lymphopenia pathology, Mice, Mice, Inbred C57BL, Mice, Transgenic, Protein Kinase C beta, Protein Kinases biosynthesis, Protein Kinases genetics, Protein Kinases metabolism, Protein Serine-Threonine Kinases, Receptors, Antigen, B-Cell physiology, B-Lymphocytes cytology, B-Lymphocytes enzymology, Growth Inhibitors physiology, NF-kappa B metabolism, Protein Kinase C metabolism, Protein Kinases physiology
Abstract

Protein kinase C-associated kinase (PKK)/receptor interacting protein 4 (RIP4) is a protein kinase C (PKC) beta-associated kinase that links PKC to NF-kappaB activation. The kinase domain of PKK is similar to that of RIP, RIP2, and RIP3. We show in this study that PKK is expressed early during lymphocyte development and can be detected in common lymphoid progenitor cells. Targeting of a catalytically inactive version of PKK to lymphoid cells resulted in a marked impairment in pro-B cell generation in the bone marrow. Although peripheral B cell numbers were markedly reduced, differentiation into follicular and marginal zone B cells was not defective in these mice. B-1a and B-1b B cells could not be detected in these mice, but this might be a reflection of the overall defect in B cell production observed in these animals. In keeping with a possible link to PKCbeta, peripheral B cells in these mice exhibit a defect in anti-IgM-mediated proliferation. These studies suggest that PKK may be required early in B cell development and for BCR-mediated B cell proliferation.

Published
2003
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