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136 results on '"Cheng, Hwei-Ling"'

1. Vaccination induces broadly neutralizing antibody precursors to HIV gp41

Author

Schiffner, Torben, Phung, Ivy, Ray, Rashmi, Irimia, Adriana, Tian, Ming, Swanson, Olivia, Lee, Jeong Hyun, Lee, Chang-Chun D., Marina-Zárate, Ester, Cho, So Yeon, Huang, Jiachen, Ozorowski, Gabriel, Skog, Patrick D., Serra, Andreia M., Rantalainen, Kimmo, Allen, Joel D., Baboo, Sabyasachi, Rodriguez, Oscar L., Himansu, Sunny, Zhou, Jianfu, Hurtado, Jonathan, Flynn, Claudia T., McKenney, Katherine, Havenar-Daughton, Colin, Saha, Swati, Shields, Kaitlyn, Schultze, Steven, Smith, Melissa L., Liang, Chi-Hui, Toy, Laura, Pecetta, Simone, Lin, Ying-Cing, Willis, Jordan R., Sesterhenn, Fabian, Kulp, Daniel W., Hu, Xiaozhen, Cottrell, Christopher A., Zhou, Xiaoya, Ruiz, Jennifer, Wang, Xuesong, Nair, Usha, Kirsch, Kathrin H., Cheng, Hwei-Ling, Davis, Jillian, Kalyuzhniy, Oleksandr, Liguori, Alessia, Diedrich, Jolene K., Ngo, Julia T., Lewis, Vanessa, Phelps, Nicole, Tingle, Ryan D., Spencer, Skye, Georgeson, Erik, Adachi, Yumiko, Kubitz, Michael, Eskandarzadeh, Saman, Elsliger, Marc A., Amara, Rama R., Landais, Elise, Briney, Bryan, Burton, Dennis R., Carnathan, Diane G., Silvestri, Guido, Watson, Corey T., Yates, III, John R., Paulson, James C., Crispin, Max, Grigoryan, Gevorg, Ward, Andrew B., Sok, Devin, Alt, Frederick W., Wilson, Ian A., Batista, Facundo D., Crotty, Shane, and Schief, William R.

Published
2024
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2. Author Correction: Vaccination induces broadly neutralizing antibody precursors to HIV gp41

Author

Schiffner, Torben, Phung, Ivy, Ray, Rashmi, Irimia, Adriana, Tian, Ming, Swanson, Olivia, Lee, Jeong Hyun, Lee, Chang-Chun D., Marina-Zárate, Ester, Cho, So Yeon, Huang, Jiachen, Ozorowski, Gabriel, Skog, Patrick D., Serra, Andreia M., Rantalainen, Kimmo, Allen, Joel D., Baboo, Sabyasachi, Rodriguez, Oscar L., Himansu, Sunny, Zhou, Jianfu, Hurtado, Jonathan, Flynn, Claudia T., McKenney, Katherine, Havenar-Daughton, Colin, Saha, Swati, Shields, Kaitlyn, Schultze, Steven, Smith, Melissa L., Liang, Chi-Hui, Toy, Laura, Pecetta, Simone, Lin, Ying-Cing, Willis, Jordan R., Sesterhenn, Fabian, Kulp, Daniel W., Hu, Xiaozhen, Cottrell, Christopher A., Zhou, Xiaoya, Ruiz, Jennifer, Wang, Xuesong, Nair, Usha, Kirsch, Kathrin H., Cheng, Hwei-Ling, Davis, Jillian, Kalyuzhniy, Oleksandr, Liguori, Alessia, Diedrich, Jolene K., Ngo, Julia T., Lewis, Vanessa, Phelps, Nicole, Tingle, Ryan D., Spencer, Skye, Georgeson, Erik, Adachi, Yumiko, Kubitz, Michael, Eskandarzadeh, Saman, Elsliger, Marc A., Amara, Rama R., Landais, Elise, Briney, Bryan, Burton, Dennis R., Carnathan, Diane G., Silvestri, Guido, Watson, Corey T., Yates, III, John R., Paulson, James C., Crispin, Max, Grigoryan, Gevorg, Ward, Andrew B., Sok, Devin, Alt, Frederick W., Wilson, Ian A., Batista, Facundo D., Crotty, Shane, and Schief, William R.

Published
2024
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5. Stress-Dependent Regulation of FOXO Transcription Factors by the SIRT1 Deacetylase

Author

Brunet, Anne, Sweeney, Lora B., Sturgill, J. Fitzhugh, Chua, Katrin F., Greer, Paul L., Lin, Yingxi, Tran, Hien, Ross, Sarah E., Mostoslavsky, Raul, Cohen, Haim Y., Hu, Linda S., Cheng, Hwei-Ling, Jedrychowski, Mark P., Gygi, Steven P., Sinclair, David A., Alt, Frederick W., and Greenberg, Michael E.

Published
2004

10. Homozygous DNA Ligase IV R278H Mutation in Mice Leads to Leaky SCID and Represents a Model for Human LIG4 Syndrome

Author

Rucci, Francesca, Notarangelo, Luigi D., Fazeli, Alex, Patrizi, Laura, Hickernell, Thomas, Paganini, Tiziana, Coakley, Kristen M., Detre, Cynthia, Keszei, Marton, Walter, Jolan E., Feldman, Lauren, Cheng, Hwei-Ling, Poliani, Pietro Luigi, Wang, Jing H., Balter, Barbara B., Recher, Mike, Andersson, Emma-Maria, Zha, Shan, Giliani, Silvia, Terhorst, Cox, Alt, Frederick W., and Yan, Catherine T.

Published
2010
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14. The NAD-dependent deacetylase SIRT2 is required for programmed necrosis

Author

Narayan, Nisha, Lee, In Hye, Borenstein, Ronen, Sun, Junhui, Wong, Renee, Tong, Guang, Fergusson, Maria M., Liu, Jie, Rovira, Ilsa I., Cheng, Hwei-Ling, Wang, Guanghui, Gucek, Marjan, Lombard, David, Alt, Fredrick W., Sack, Michael N., Murphy, Elizabeth, Cao, Liu, and Finkel, Toren

Subjects
Enzymes -- Properties -- Testing, Cellular control mechanisms -- Research, Necrosis -- Observations, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Although initially viewed as unregulated, increasing evidence suggests that cellular necrosis often proceeds through a specific molecular program. In particular, death ligands such as tumour necrosis factor (TNF)-α activate necrosis by stimulating the formation of a complex containing receptor-interacting protein 1 (RIP1) and receptor-interacting protein 3 (RIP3). Relatively little is known regarding how this complex formation is regulated. Here, we show that the NAD-dependent deacetylase SIRT2 binds constitutively to RIP3 and that deletion or knockdown of SIRT2 prevents formation of the RIP1-RIP3 complex in mice. Furthermore, genetic or pharmacological inhibition of SIRT2 blocks cellular necrosis induced by TNF-α. We further demonstrate that RIP1 is a critical target of SIRT2-dependent deacetylation. Using gain- and loss-of-function mutants, we demonstrate that acetylation of RIP1 lysine 530 modulates RIP1-RIP3 complex formation and TNF-a-stimulated necrosis. In the setting of ischaemia-reperfusion injury, RIP1 is deacetylated in a SIRT2-dependent fashion. Furthermore, the hearts of [Sirt2.sup.-/-] mice, or wild- type mice treated with a specific pharmacological inhibitor of SIRT2, show marked protection from ischaemic injury. Taken together, these results implicate SIRT2 as an important regulator of programmed necrosis and indicate that inhibitors of this deacetylase may constitute a novel approach to protect against necrotic injuries, including ischaemic stroke and myocardial infarction., Several forms of cell death exist, each showing distinctive morphological features. The apoptotic program is an energy-dependent method of cell death that results in cytoplasmic shrinking, nuclear condensation, caspase activation [...]

Published
2012
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15. CTCF-binding elements mediate control of V(D)J recombination

Author

Guo, Chunguang, Yoon, Hye Suk, Franklin, Andrew, Jain, Suvi, Ebert, Anja, Cheng, Hwei-Ling, Hansen, Erica, Despo, Orion, Bossen, Claudia, Vettermann, Christian, Bates, Jamie G., Richards, Nicholas, Myers, Darienne, Patel, Harin, Gallagher, Michael, Schlissel, Mark S., Murre, Cornelis, Busslinger, Meinrad, Giallourakis, Cosmas C., and Alt, Frederick W.

Subjects
Zinc finger proteins -- Properties, Immunoglobulins -- Properties, Protein binding -- Research, Cell development (Biology) -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Immunoglobulin heavy chain (IgH) variable region exons are assembled from VH, D and JH gene segments in developing B lymphocytes. Within the 2.7-megabase mouse Igh locus, V(D)J recombination is regulated to ensure specific and diverse antibody repertoires. Here we report in mice a key Igh V(D)J recombination regulatory region, termed intergenic control region 1 (IGCR1), which lies between the [V.sub.H] and D clusters. Functionally, IGCR1 uses CTCF looping/insulator factor-binding elements and, correspondingly, mediates Igh loops containing distant enhancers. IGCR1 promotes normal B-cell development and balances antibody repertoires by inhibiting transcription and rearrangement of [D.sub.H]-proximal [V.sub.H] gene segments and promoting rearrangement of distal [V.sub.H] segments. IGCR1 maintains ordered and lineage-specific [V.sub.H](D)[J.sub.H] recombination by suppressing [V.sub.H] joining to D segments not joined to [J.sub.H] segments, and [V.sub.H] to D[J.sub.H] joins in thymocytes, respectively. IGCR1 is also required for feedback regulation and allelic exclusion of proximal [V.sub.H]-to-D[J.sub.H] recombination. Our studies elucidate a long-sought Igh V(D)J recombination control region and indicate a new role for the generally expressed CTCF protein., The variable region exons of IgH, Ig light (IgL) and T-cell receptor genes are assembled during B- or T-cell development from variable (V), diversity (D) and joining (J) gene segments [...]

Published
2011
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16. ATM damage response and XLF repair factor are functionally redundant in joining DNA breaks

Author

Zha, Shan, Guo, Chunguang, Boboila, Cristian, Oksenych, Valentyn, Cheng, Hwei-Ling, Zhang, Yu, Wesemann, Duane R., Yuen, Grace, Patel, Harin, Goff, Peter H., Dubois, Richard L., and Alt, Frederick W.

Subjects
Ataxia telangiectasia -- Diagnosis -- Care and treatment, DNA damage -- Causes of -- Care and treatment, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Classical non-homologous DNA end-joining (NHEJ) is a major mammalian DNA double-strand-break (DSB) repair pathway. Deficiencies for classical NHEJ factors, such as XRCC4, abrogate lymphocyte development, owing to a strict requirement for classical NHEJ to join V(D)J recombination DSB intermediates (1,2). The XRCC4-like factor (XLF; also called NHEJ1) is mutated in certain immunodeficient human patients and has been implicated in classical NHEJ (3-6); however, XLF-deficient mice have relatively normal lymphocyte development and their lymphocytes support normal V(D)J recombination (5). The ataxia telangiectasia-mutated protein (ATM) detects DSBs and activates DSB responses by phosphorylating substrates including histone H2AX (7). However, ATM deficiency causes only modest V(D)J recombination and lymphocyte developmental defects, and H2AX deficiency does not have a measurable impact on these processes (7-9). Here we show that XLF, ATM and H2AX all have fundamental roles in processing and joining DNA ends during V(D)J recombination, but that these roles have been masked by unanticipated functional redundancies. Thus, combined deficiency of ATM and XLF nearly blocks mouse lymphocyte development due to an inability to process and join chromosomal V(D)J recombination DSB intermediates. Combined XLF and ATM deficiency also severely impairs classical NHEJ, but not alternative end-joining, during IgH class switch recombination. Redundant ATM and XLF functions in classical NHEJ are mediated by ATM kinase activity and are not required for extra-chromosomal V(D)J recombination, indicating a role for chromatin-associated ATM substrates. Correspondingly, conditional H2AX inactivation in XLF-deficient pro-B lines leads to V(D)J recombination defects associated with marked degradation of unjoined V(D)J ends, revealing that H2AX has a role in this process., Assembly of immunoglobulin and T-cell-receptor variable region exons is initiated by the RAG1 and RAG2 endonuclease (hereafter referred to as RAG), which generates DNA DSBs between a pair of participating [...]

Published
2011
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18. Conditional Antibody Expression to Avoid Central B Cell Deletion in a Humanized HIV-1 Vaccine Mouse Models

Author

Tian, Ming, primary, McGovern, Kelly, additional, Cheng, Hwei-Ling, additional, Waddicor, Peyton, additional, Rieble, Lisa, additional, Dao, Mai, additional, Chen, Yiwei, additional, Kimble, Michael T., additional, Cantor, Elizabeth, additional, Manfredonia, Nicole, additional, Judson, Rachael, additional, Chapdelaine-Williams, Aimee, additional, Cain, Derek W., additional, Haynes, Barton F., additional, and Alt, Frederick W., additional

Published
2020
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19. Targeted selection of HIV-specific antibody mutations by engineering B cell maturation

Author

Saunders, Kevin O., primary, Wiehe, Kevin, additional, Tian, Ming, additional, Acharya, Priyamvada, additional, Bradley, Todd, additional, Alam, S. Munir, additional, Go, Eden P., additional, Scearce, Richard, additional, Sutherland, Laura, additional, Henderson, Rory, additional, Hsu, Allen L., additional, Borgnia, Mario J., additional, Chen, Haiyan, additional, Lu, Xiaozhi, additional, Wu, Nelson R., additional, Watts, Brian, additional, Jiang, Chuancang, additional, Easterhoff, David, additional, Cheng, Hwei-Ling, additional, McGovern, Kelly, additional, Waddicor, Peyton, additional, Chapdelaine-Williams, Aimee, additional, Eaton, Amanda, additional, Zhang, Jinsong, additional, Rountree, Wes, additional, Verkoczy, Laurent, additional, Tomai, Mark, additional, Lewis, Mark G., additional, Desaire, Heather R., additional, Edwards, Robert J., additional, Cain, Derek W., additional, Bonsignori, Mattia, additional, Montefiori, David, additional, Alt, Frederick W., additional, and Haynes, Barton F., additional

Published
2019
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21. Late embryonic lethality and impaired V(D)J recombination in mice lacking DNA ligase IV

Author

Frank, Karen M., Sekiguchi, JoAnn M., Seidl, Katherine J., Swat, Wojciech, Rathbun, Gary A., Cheng, Hwei-Ling, Davidson, Laurie, Kangaloo, Landy, and Alt, Frederick W.

Subjects
Ligases -- Research, Protein kinases -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

DNA-end-joining reactions used in repair have common factors, including components of DNA-dependent protein kinase (DNA-PK), and Ku70-Ku80- and XRCC4. XRCC5 is known to interact with DNA ligase IV. The inactivation of the ligase IV gene in mice is shown to result in late embryonic lethality. V(D)J joining does not occur and ligase IV-deficient embryonic fibroblasts are sensitive to ionizing radiation, premature senescence and growth defects.

Published
1998

22. Activated Ras signals differentiation and expansion of CD4+8+ thymocytes

Author

Swat, Wojciech, Shinkai, Yoichi, Cheng, Hwei-Ling, Davidson, Laurie, and Alt, Frederick W.

Subjects
Ras genes -- Research, CD4 lymphocytes -- Research, CD8 lymphocytes -- Research, T cells -- Research, Cellular signal transduction -- Research, Science and technology
Abstract

We describe a novel approach to assay the ability of particular gene products to signal transitions in lymphocyte differention in vivo. The method involves transfection of test expression constructs into RAG-1-deficient embryonic stem cells, which are subsequently assayed by the RAG-2-deficient blastocyst complementation approach. We have used this method to demonstrate that expression of activated Ras in CD[4.sup.-][8.sup.-] (double negative, DN) prothymocytes in vivo induces their differentiation into small CD[4.sup.+][8.sup.+] (double positive, DP) cortical thymocytes with accompanying expansion to normal thymocyte numbers. However, activated Ras expression in DP cells does not cause proliferation or maturation to CD[4.sup.+][8.sup.-] or CD[4.sup.-][8.sup.+] (single positive) thymocytes. Therefore, signaling through Ras is sufficient for promoting differentiation of DN to DP cells, but further differentiation requires the activity of additional signaling pathways.

Published
1996

23. The XRCC4 gene encodes a novel protein involved in DNA double-strand break repair and V(D)J recombination

Author

Li, Zhiying, Otevrel, Tomas, Gao, Yijie, Cheng, Hwei-Ling, Seed, Brian, Stamato, Thomas D., Taccioli, Guillermo E., and Alt, Frederick W.

Subjects
DNA repair -- Research, Genetic recombination -- Research, Gene expression -- Research, Biological sciences
Abstract

The protein encoded by the XRCC4 gene is necessary for double-strand break repair (DSBR) and V(D)J recombination. The XR-1 ovary cell line without the XRCC4 gene initiates V(D)J recombination but fails to form coding and recognition sequence links. The expression of the XRCC4 gene in XR-1 cells restores the V(D)J recombination ability. The DSBR ability is partially restored, probably due to the existence of an XRCC4-independent DSBR pathway.

Published
1995

25. A class switch control region at the 3' end of the immunoglobulin heavy chain locus

Author

Cogne, Michel, Lansford, Rusty, Bottaro, Andrea, Zhang, Jue, Gorman, James, Young, Faith, Cheng, Hwei-Ling, and Alt, Frederick W.

Subjects
Immunoglobulins -- Research, Mutation (Biology) -- Analysis, Biological sciences
Abstract

A mutation of the homozygous IgH3' enhancer (3'EH+/-) in ES cells affects the region involved in heavy chain class switching. The effects, both in vitro and in vivo, extend upto 100 kb upstream of the mutated region. 3'EH is involved in activities such as transcription and somatic mutation of the IgH locus.

Published
1994

26. Induction of HIV Neutralizing Antibody Lineages in Mice with Diverse Precursor Repertoires

Author

Tian, Ming, primary, Cheng, Cheng, additional, Chen, Xuejun, additional, Duan, Hongying, additional, Cheng, Hwei-Ling, additional, Dao, Mai, additional, Sheng, Zizhang, additional, Kimble, Michael, additional, Wang, Lingshu, additional, Lin, Sherry, additional, Schmidt, Stephen D., additional, Du, Zhou, additional, Joyce, M. Gordon, additional, Chen, Yiwei, additional, DeKosky, Brandon J., additional, Chen, Yimin, additional, Normandin, Erica, additional, Cantor, Elizabeth, additional, Chen, Rita E., additional, Doria-Rose, Nicole A., additional, Zhang, Yi, additional, Shi, Wei, additional, Kong, Wing-Pui, additional, Choe, Misook, additional, Henry, Amy R., additional, Laboune, Farida, additional, Georgiev, Ivelin S., additional, Huang, Pei-Yi, additional, Jain, Suvi, additional, McGuire, Andrew T., additional, Georgeson, Eric, additional, Menis, Sergey, additional, Douek, Daniel C., additional, Schief, William R., additional, Stamatatos, Leonidas, additional, Kwong, Peter D., additional, Shapiro, Lawrence, additional, Haynes, Barton F., additional, Mascola, John R., additional, and Alt, Frederick W., additional

Published
2016
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27. Retraction: the NAD-dependent deacetylase SIRT2 is required for programmed necrosis

Author

Narayan, Nisha, Lee, In Hye, Borenstein, Ronen, Sun, Junhui, Wong, Renee, Tong, Guang, Fergusson, Maria M., Liu, Jie, Rovira, Ilsa I., Cheng, Hwei-Ling, Wang, Guanghui, Gucek, Marjan, Lombard, David, Alt, Fredrick W., Sack, Michael N., Murphy, Elizabeth, Cao, Liu, and Finkel, Toren

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Nature 492, 199-204 (2012); doi:10.1038/nature11700 We retract this Article because some of the data, specifically the data reported in Fig. 2 demonstrating an in vitro requirement for Sirt2 in TNF-α-mediated [...]

Published
2014
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28. Retraction Note: The NAD-dependent deacetylase SIRT2 is required for programmed necrosis

Author

Narayan, Nisha, primary, Lee, In Hye, additional, Borenstein, Ronen, additional, Sun, Junhui, additional, Wong, Renee, additional, Tong, Guang, additional, Fergusson, Maria M., additional, Liu, Jie, additional, Rovira, Ilsa I., additional, Cheng, Hwei-Ling, additional, Wang, Guanghui, additional, Gucek, Marjan, additional, Lombard, David, additional, Alt, Fredrick W., additional, Sack, Michael N., additional, Murphy, Elizabeth, additional, Cao, Liu, additional, and Finkel, Toren, additional

Published
2014
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29. SIRT7 Represses Myc Activity to Suppress ER Stress and Prevent Fatty Liver Disease

Author

Shin, Jiyung, primary, He, Ming, additional, Liu, Yufei, additional, Paredes, Silvana, additional, Villanova, Lidia, additional, Brown, Katharine, additional, Qiu, Xiaolei, additional, Nabavi, Noushin, additional, Mohrin, Mary, additional, Wojnoonski, Kathleen, additional, Li, Patrick, additional, Cheng, Hwei-Ling, additional, Murphy, Andrew J., additional, Valenzuela, David M., additional, Luo, Hanzhi, additional, Kapahi, Pankaj, additional, Krauss, Ronald, additional, Mostoslavsky, Raul, additional, Yancopoulos, George D., additional, Alt, Frederick W., additional, Chua, Katrin F., additional, and Chen, Danica, additional

Published
2013
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30. The ARID Family Transcription Factor Bright Is Required for both Hematopoietic Stem Cell and B Lineage Development

Author

Webb, Carol F., primary, Bryant, James, additional, Popowski, Melissa, additional, Allred, Laura, additional, Kim, Dongkoon, additional, Harriss, June, additional, Schmidt, Christian, additional, Miner, Cathrine A., additional, Rose, Kira, additional, Cheng, Hwei-Ling, additional, Griffin, Courtney, additional, and Tucker, Philip W., additional

Published
2011
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35. Mice Lacking Histone Deacetylase 6 Have Hyperacetylated Tubulin but Are Viable and Develop Normally

Author

Zhang, Yu, primary, Kwon, SoHee, additional, Yamaguchi, Teppei, additional, Cubizolles, Fabien, additional, Rousseaux, Sophie, additional, Kneissel, Michaela, additional, Cao, Chun, additional, Li, Na, additional, Cheng, Hwei-Ling, additional, Chua, Katrin, additional, Lombard, David, additional, Mizeracki, Adam, additional, Matthias, Gabriele, additional, Alt, Frederick W., additional, Khochbin, Saadi, additional, and Matthias, Patrick, additional

Published
2008
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36. OR.1. Hypomorphic Rag1 and Lig4 Mutants are a Model for Human Leaky SCID

Author

Rucci, Francesca, primary, Poliani, Pietro, additional, Yan, Catherine, additional, Sekiguchi, JoAnn, additional, Cheng, Hwei-Ling, additional, Caraffi, Stefano, additional, De La Fuente, Miguel, additional, Walter, Jolan, additional, Facchetti, Fabio, additional, Villa, Anna, additional, Alt, Frederick, additional, and Notarangelo, Luigi, additional

Published
2008
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37. Mammalian Sir2 Homolog SIRT3 Regulates Global Mitochondrial Lysine Acetylation

Author

Lombard, David B., primary, Alt, Frederick W., additional, Cheng, Hwei-Ling, additional, Bunkenborg, Jakob, additional, Streeper, Ryan S., additional, Mostoslavsky, Raul, additional, Kim, Jennifer, additional, Yancopoulos, George, additional, Valenzuela, David, additional, Murphy, Andrew, additional, Yang, Yinhua, additional, Chen, Yaohui, additional, Hirschey, Matthew D., additional, Bronson, Roderick T., additional, Haigis, Marcia, additional, Guarente, Leonard P., additional, Farese, Robert V., additional, Weissman, Sherman, additional, Verdin, Eric, additional, and Schwer, Bjoern, additional

Published
2007
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39. Genomic Instability and Aging-like Phenotype in the Absence of Mammalian SIRT6

Author

Mostoslavsky, Raul, primary, Chua, Katrin F., additional, Lombard, David B., additional, Pang, Wendy W., additional, Fischer, Miriam R., additional, Gellon, Lionel, additional, Liu, Pingfang, additional, Mostoslavsky, Gustavo, additional, Franco, Sonia, additional, Murphy, Michael M., additional, Mills, Kevin D., additional, Patel, Parin, additional, Hsu, Joyce T., additional, Hong, Andrew L., additional, Ford, Ethan, additional, Cheng, Hwei-Ling, additional, Kennedy, Caitlin, additional, Nunez, Nomeli, additional, Bronson, Roderick, additional, Frendewey, David, additional, Auerbach, Wojtek, additional, Valenzuela, David, additional, Karow, Margaret, additional, Hottiger, Michael O., additional, Hursting, Stephen, additional, Barrett, J. Carl, additional, Guarente, Leonard, additional, Mulligan, Richard, additional, Demple, Bruce, additional, Yancopoulos, George D., additional, and Alt, Frederick W., additional

Published
2006
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42. Growth Retardation and Leaky SCID Phenotype of Ku70-Deficient Mice

Author

Gu, Yansong, primary, Seidl, Katherine J, additional, Rathbun, Gary A, additional, Zhu, Chengming, additional, Manis, John P, additional, van der Stoep, Nienke, additional, Davidson, Laurie, additional, Cheng, Hwei-Ling, additional, Sekiguchi, JoAnn M, additional, Frank, Karen, additional, Stanhope-Baker, Patricia, additional, Schlissel, Mark S, additional, Roth, David B, additional, and Alt, Frederick W, additional

Published
1997
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46. Mouse spleen and IgD-secreting plasmacytomas contain multiple IgD δ chain RNAs

Author

Fitzmaurice, Leona, Owens, James, Blattner, Frederick R., Cheng, Hwei-Ling, Tucker, Philip W., and Mushinski, J. Frederic

Abstract

Immunoglobulin gene expression requires that cells combine the correct genetic information by DNA rearrangement and RNA processing to produce mature, translatable mRNAs. The mechanisms that operate to produce IgD heavy chain (δ chain) mRNA are thought to be especially complex1–3. Like other immunoglobulins, IgD exists in membrane and secreted forms4,5. By analogy with results of studies of μ6–10and γ11,12gene expression, we expected that δ chains would also be encoded by two different mRNAs, containing common sequence information transcribed from constant region gene segments but different information transcribed from coding sequences located 3′ to the constant region gene segments. Instead, we identified13more than two δ mRNAs in normal mouse spleen and in two IgD-secreting plasmacytomas14, TEPC 1017 and TEPC 1033. Now we have used 32P-labelled DNA fragments prepared from a δ cDNA clone15and a δ genomic clone16to characterize by hybridization these δ RNAs, fractionated on methyl mercury hydroxide agarose gels. We find that normal mouse spleen contains a major 2.9-kilobase (kb) and a minor 2.1-kb RNA encoding membrane-bound δ chains (δm) and that TEPC 1017 and TEPC 1033 contain similar δmRNAs plus a 1.75-kb RNA encoding secreted δ chains (δm). We have also observed less abundant δ RNA species (2.65 and 3.2 kb). Different gene segments or combinations of segments are used in the 3′ termini of the multiple δ RNAs.

Published
1982
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47. Structure of genes for membrane and secreted murine IgD heavy chains

Author

Cheng, Hwei-Ling, Blattner, Frederick R., Fitzmaurice, Leona, Mushinski, J. Frederic, and Tucker, Philip W.

Abstract

We have sequenced secreted and membrane terminal exons of the murine immunoglobulin δ chain. The putative transmembranal exon is strikingly similar to that of the μ chain and the internal cytoplasmic exon codes for exactly the same two amino acids, valine and lysine. A third potential exon was found between S and M exons that could code for yet another hydrophilic carboxyl terminus termed δX.

Published
1982
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48. An efficient and general method for sequencing immunoglobulin mRNAs

Author

Sood, Ashwani K., Cheng, Hwei-Ling, and Kohler, Heinz

Abstract

By using two oligonucleotide primers, one complementary to a short DNA segment in the first constant region exon and second complementary to a short segment in the variable region, we have developed a highly efficient method for sequencing immunoglobulin mRNAs. Using the first primer full length immunoglobulin-specific cDNA was synthesized and separated on a denaturing acrylamide/urea gel. The desired band was isolated from the gel and sequenced by Maxam/Gilbert method. Using the sequence generated, a second oligonucleotide primer complementary to a short segment in the variable region was synthesized and similarly used to complete the remaining sequence of the variable region, the signal peptide and the 5′-untranslated region.

Published
1986
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