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3. GIMAP5 deficiency reveals a mammalian ceramide-driven longevity assurance pathway

Author

Park, Ann Y., Leney-Greene, Michael, Lynberg, Matthew, Gabrielski, Justin Q., Xu, Xijin, Schwarz, Benjamin, Zheng, Lixin, Balasubramaniyam, Arasu, Ham, Hyoungjun, Chao, Brittany, Zhang, Yu, Matthews, Helen F., Cui, Jing, Yao, Yikun, Kubo, Satoshi, Chanchu, Jean Michel, Morawski, Aaron R., Cook, Sarah A., Jiang, Ping, Ravell, Juan C., Cheng, Yan H., George, Alex, Faruqi, Aiman, Pagalilauan, Alison M., Bergerson, Jenna R. E., Ganesan, Sundar, Chauvin, Samuel D., Aluri, Jahnavi, Edwards-Hicks, Joy, Bohrnsen, Eric, Tippett, Caroline, Omar, Habib, Xu, Leilei, Butcher, Geoffrey W., Pascall, John, Karakoc-Aydiner, Elif, Kiykim, Ayca, Maecker, Holden, Tezcan, İlhan, Esenboga, Saliha, Heredia, Raul Jimenez, Akata, Deniz, Tekin, Saban, Kara, Altan, Kuloglu, Zarife, Unal, Emel, Kendirli, Tanıl, Dogu, Figen, Karabiber, Esra, Atkinson, T. Prescott, Cochet, Claude, Filhol, Odile, Bosio, Catherine M., Davis, Mark M., Lifton, Richard P., Pearce, Erika L., Daumke, Oliver, Aytekin, Caner, Şahin, Gülseren Evirgen, Aksu, Aysel Ünlüsoy, Uzel, Gulbu, Koneti Rao, V., Sari, Sinan, Dalgıç, Buket, Boztug, Kaan, Cagdas, Deniz, Haskologlu, Sule, Ikinciogullari, Aydan, Schwefel, David, Vilarinho, Silvia, Baris, Safa, Ozen, Ahmet, Su, Helen C., and Lenardo, Michael J.

Published
2024
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24. Author Correction: GIMAP5 deficiency reveals a mammalian ceramide-driven longevity assurance pathway

Author

Park, Ann Y., Leney-Greene, Michael, Lynberg, Matthew, Gabrielski, Justin Q., Xu, Xijin, Schwarz, Benjamin, Zheng, Lixin, Balasubramaniyam, Arasu, Ham, Hyoungjun, Chao, Brittany, Zhang, Yu, Matthews, Helen F., Cui, Jing, Yao, Yikun, Kubo, Satoshi, Chanchu, Jean Michel, Morawski, Aaron R., Cook, Sarah A., Jiang, Ping, Ravell, Juan C., Cheng, Yan H., George, Alex, Faruqi, Aiman, Pagalilauan, Alison M., Bergerson, Jenna R. E., Ganesan, Sundar, Chauvin, Samuel D., Aluri, Jahnavi, Edwards-Hicks, Joy, Bohrnsen, Eric, Tippett, Caroline, Omar, Habib, Xu, Leilei, Butcher, Geoffrey W., Pascall, John, Karakoc-Aydiner, Elif, Kiykim, Ayca, Maecker, Holden, Tezcan, İlhan, Esenboga, Saliha, Heredia, Raul Jimenez, Akata, Deniz, Tekin, Saban, Kara, Altan, Kuloglu, Zarife, Unal, Emel, Kendirli, Tanıl, Dogu, Figen, Karabiber, Esra, Atkinson, T. Prescott, Cochet, Claude, Filhol, Odile, Bosio, Catherine M., Davis, Mark M., Lifton, Richard P., Pearce, Erika L., Daumke, Oliver, Aytekin, Caner, Şahin, Gülseren Evirgen, Aksu, Aysel Ünlüsoy, Uzel, Gulbu, Koneti Rao, V., Sari, Sinan, Dalgıç, Buket, Boztug, Kaan, Cagdas, Deniz, Haskologlu, Sule, Ikinciogullari, Aydan, Schwefel, David, Vilarinho, Silvia, Baris, Safa, Ozen, Ahmet, Su, Helen C., and Lenardo, Michael J.

Published
2024
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28. Synergistically creating sulfur vacancies in semimetal-supported amorphous MoS2 for efficient hydrogen evolution

Author

Li, Guowei, Fu, Chenguang, Wu, Jiquan, Rao, Jiancun, Liou, Sz-Chian, Xu, Xijin, Shao, Baiqi, Liu, Kai, Liu, Enke, Kumar, Nitesh, Liu, Xianjie, Fahlman, Mats, Gooth, Johannes, Auffermann, Gudrun, Sun, Yan, Felser, Claudia, and Zhang, Baomin

Subjects
Condensed Matter - Materials Science
Abstract

The presence of elemental vacancies in materials is inevitable according to statistical thermodynamics, which will decide the chemical and physical properties of the investigated system. However, the controlled manipulation of vacancies for specific applications is a challenge. Here we report a facile method for creating large concentrations of S vacancies in the inert basal plane of MoS2 supported on semimetal CoMoP2. With a small applied potential, S atoms can be removed in the form of H2S due to the optimized free energy of formation. The existence of vacancies favors electron injection from the electrode to the active site by decreasing the contact resistance. As a consequence, the activity is increased by 221 % with the vacancy-rich MoS2 as electrocatalyst for hydrogen evolution reaction (HER). A small overpotential of 75 mV is needed to deliver a current density of 10 mA cm-2, which is considered among the best values achieved for MoS2. It is envisaged that this work may provide a new strategy for utilizing the semimetal phase for structuring MoS2 into a multi-functional material.

Published
2020

48. An essential role for the Zn2+ transporter ZIP7 in B cell development

Author

Anzilotti, Consuelo, Swan, David J, Boisson, Bertrand, Deobagkar-Lele, Mukta, Oliveira, Catarina, Chabosseau, Pauline, Engelhardt, Karin R, Xu, Xijin, Chen, Rui, Alvarez, Luis, Berlinguer-Palmini, Rolando, Bull, Katherine R, Cawthorne, Eleanor, Cribbs, Adam P, Crockford, Tanya L, Dang, Tarana Singh, Fearn, Amy, Fenech, Emma J, de Jong, Sarah J, Lagerholm, B Christoffer, Ma, Cindy S, Sims, David, van den Berg, Bert, Xu, Yaobo, Cant, Andrew J, Kleiner, Gary, Leahy, T Ronan, de la Morena, M Teresa, Puck, Jennifer M, Shapiro, Ralph S, van der Burg, Mirjam, Chapman, J Ross, Christianson, John C, Davies, Benjamin, McGrath, John A, Przyborski, Stefan, Santibanez Koref, Mauro, Tangye, Stuart G, Werner, Andreas, Rutter, Guy A, Padilla-Parra, Sergi, Casanova, Jean-Laurent, Cornall, Richard J, Conley, Mary Ellen, and Hambleton, Sophie

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Prevention, Genetics, Brain Disorders, Underpinning research, Aetiology, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Agammaglobulinemia, Animals, B-Lymphocytes, Cation Transport Proteins, Child, Preschool, Cytosol, Disease Models, Animal, Endoplasmic Reticulum, Female, Gene Expression Profiling, Humans, Infant, Male, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Pedigree, Zinc, Immunology, Biochemistry and cell biology
Abstract

Despite the known importance of zinc for human immunity, molecular insights into its roles have remained limited. Here we report a novel autosomal recessive disease characterized by absent B cells, agammaglobulinemia and early onset infections in five unrelated families. The immunodeficiency results from hypomorphic mutations of SLC39A7, which encodes the endoplasmic reticulum-to-cytoplasm zinc transporter ZIP7. Using CRISPR-Cas9 mutagenesis we have precisely modeled ZIP7 deficiency in mice. Homozygosity for a null allele caused embryonic death, but hypomorphic alleles reproduced the block in B cell development seen in patients. B cells from mutant mice exhibited a diminished concentration of cytoplasmic free zinc, increased phosphatase activity and decreased phosphorylation of signaling molecules downstream of the pre-B cell and B cell receptors. Our findings highlight a specific role for cytosolic Zn2+ in modulating B cell receptor signal strength and positive selection.

Published
2019

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