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1. Two predicted α-helices within the prion-like domain of TIAR-1 play a crucial role in its association with stress granules in Caenorhabditis elegans

Author

D. A. Fuentes-Jiménez, L. S. Salinas, E. Morales-Oliva, V. A. Ramírez-Ramírez, M. Arciniega, and R. E. Navarro

Subjects
stress granules, TIA1, TIAR1, TIAR-1, stress, apoptosis, Biology (General), QH301-705.5
Abstract

Stress granules (SGs) are sites for mRNA storage, protection, and translation repression. TIA1 and TIAR1 are two RNA-binding proteins that are key players in SGs formation in mammals. TIA1/TIAR have a prion-like domain (PrD) in their C-terminal that promotes liquid-phase separation. Lack of any TIA1/TIAR has severe consequences in mice. However, it is not clear whether the failure to form proper SGs is the cause of any of these problems. We disrupted two predicted α-helices within the prion-like domain of the Caenohabditis elegans TIA1/TIAR homolog, TIAR-1, to test whether its association with SGs is important for the nematode. We found that tiar-1 PrD mutant animals continued to form TIAR-1 condensates under stress in the C. elegans gonad. Nonetheless, TIAR-1 condensates appeared fragile and disassembled quickly after stress. Apparently, the SGs continued to associate regularly as observed with CGH-1, an SG marker. Like tiar-1-knockout nematodes, tiar-1 PrD mutant animals exhibited fertility problems and a shorter lifespan. Notwithstanding this, tiar-1 PrD mutant nematodes were no sensitive to stress. Our data demonstrate that the predicted prion-like domain of TIAR-1 is important for its association with stress granules. Moreover, this domain may also play a significant role in various TIAR-1 functions unrelated to stress, such as fertility, embryogenesis and lifespan.

Published
2023
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2. Apoptosis contributes to protect germ cells from the oogenic germline starvation response but is not essential for the gonad shrinking or recovery observed during adult reproductive diapause in C. elegans.

Author

E Carranza-García and R E Navarro

Subjects
Medicine, Science
Abstract

When C. elegans hermaphrodites are deprived of food during the mid-L4 larval stage and throughout adulthood, they enter an alternative stage termed "adult reproductive diapause (ARD)" in which they halt reproduction and extend their lifespan. During ARD, germ cell proliferation stops; oogenesis is slowed; and the gonad shrinks progressively, which has been described as the "oogenic germline starvation response". Upon refeeding, the shrunken gonad is regenerated, and animals recover fertility and live out their remaining lifespan. Little is known about the effects of ARD on oocyte quality after ARD. Thus, the aim of this study was to determine how oocyte quality is affected after ARD by measuring brood size and embryonic lethality as a reflection of defective oocyte production. We found that ARD affects reproductive capacity. The oogenic germline starvation response protects oogenic germ cells by slowing oogenesis to prevent prolonged arrest in diakinesis. In contrast to a previous report, we found that germ cell apoptosis is not the cause of gonad shrinkage; instead, we propose that ovulation contributes to gonad shrinkage during the oogenic germline starvation response. We show that germ cell apoptosis increases and continues during ARD via lin-35/Rb and an unknown mechanism. Although apoptosis contributes to maintain germ cell quality during ARD, we demonstrated that apoptosis is not essential to preserve animal fertility. Finally, we show that IIS signaling inactivation partially participates in the oogenic germline starvation response.

Published
2019
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3. Caenorhabditis elegans ATPase inhibitor factor 1 (IF1) MAI-2 preserves the mitochondrial membrane potential (Δψm) and is important to induce germ cell apoptosis.

Author

L P Fernández-Cárdenas, E Villanueva-Chimal, L S Salinas, C José-Nuñez, M Tuena de Gómez Puyou, and R E Navarro

Subjects
Medicine, Science
Abstract

When the electrochemical proton gradient is disrupted in the mitochondria, IF1 (Inhibitor Factor-1) inhibits the reverse hydrolytic activity of the F1Fo-ATP synthase, thereby allowing cells to conserve ATP at the expense of losing the mitochondrial membrane potential (Δψm). The function of IF1 has been studied mainly in different cell lines, but these studies have generated contrasting results, which have not been helpful to understand the real role of this protein in a whole organism. In this work, we studied IF1 function in Caenorhabditis elegans to understand IF1´s role in vivo. C. elegans has two inhibitor proteins of the F1Fo-ATPase, MAI-1 and MAI-2. To determine their protein localization in C. elegans, we generated translational reporters and found that MAI-2 is expressed ubiquitously in the mitochondria; conversely, MAI-1 was found in the cytoplasm and nuclei of certain tissues. By CRISPR/Cas9 genome editing, we generated mai-2 mutant alleles. Here, we showed that mai-2 mutant animals have normal progeny, embryonic development and lifespan. Contrasting with the results previously obtained in cell lines, we found no evident defects in the mitochondrial network, dimer/monomer ATP synthase ratio, ATP concentration or respiration. Our results suggest that some of the roles previously attributed to IF1 in cell lines could not reflect the function of this protein in a whole organism and could be attributed to specific cell lines or methods used to silence, knockout or overexpress this protein. However, we did observe that animals lacking IF1 had an enhanced Δψm and lower physiological germ cell apoptosis. Importantly, we found that mai-2 mutant animals must be under stress to observe the role of IF1. Accordingly, we observed that mai-2 mutant animals were more sensitive to heat shock, oxidative stress and electron transport chain blockade. Furthermore, we observed that IF1 is important to induce germ cell apoptosis under certain types of stress. Here, we propose that MAI-2 might play a role in apoptosis by regulating Δψm. Additionally, we suggest that IF1 function is mainly observed under stress and that, under physiological conditions, this protein does not play an essential role.

Published
2017
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4. Rheumatoid arthritis and other inflammatory joint diseases (human studies) (PP-036)

Author

G. P. Nolan, T. Kinoshita, C. Lam, A. Grützkau, N. Lee, M. Horiuchi, M. Mackay, T. Tomita, T. Sumida, J. Tebib, S. Ohnishi, S. Tsujimura, N. Umeda, R. Burgos-Vargas, Y. Asanuma, C. Ionita, L. Limón-Camacho, K. Yasui, J. M. Witkowski, H. Ionita, H. Kajiyama, T. Naka, S. Tominaga, F. Miyoshi, C. Schütz, S. Hirohata, H. Amuro, M. Iwamoto, I. P. Guzmán-Guzmán, N. Miyasaka, Y. Araki, D. Naysmith, E. Meugnier, J. Kong, Y. Valle, T. N. Shibata, T. J. A. Lehman, M. García-García, Y. Yoshikai, W. Lee, I. Hideya, B. Thumthanaruk, Z. Smolenska, L. Kremer, M. Lu, T. Atsumi, Y. Hwang, J. Saegusa, A. Manki, M. Soroczynska-Cybula, T. Klaiwong, L. Jiang, V. Paunescu, P. Charles, T. Wada, E. Humphreys, B. Prakken, M. Kato, J. Sibilia, H. Ozaki, K. Watanabe, F. Terabe, R. E. Navarro-Hernández, D. Hull, K. Shimamoto, H. Kataoka, H. Okazaki, K. Yokota, B. Wang, G. Mijnheer, J. L. Huang, H. Aizawa, S. Blazickova, L. Llorente, T. Kishimoto, J. Pawlowska, H. Vidal, A. Morinobu, M. Fujita, S. Abraham, T. Avčin, N. H. Fabien, A. Palfreeman, S. Castañeda, P. Taylor, X. Chang, T. Morishima, Y. Tanaka, H. Khalili, A. S. Williams, J. R. Grün, I. Gonzalez-Alvaro, Y. Nasuhara, R. Minami, T. Takii, D. Pramod, G. Manda, A. Ortiz, K. Saito, I. Matsumoto, H. Ishibashi, S. Fukuhara, P. Wu, H. Itoh, M. Mizushima, M. Nakamura, C. C. Liao, Y. Onodera, T. Koike, P. Bowness, S. Ito, J. Chen, Y. Fujieda, S. Takei, R. Amakawa, A. Radbruch, S. A. Alzabin, A. Inoue, J. Jiang, A. Ma, K. Sawai, I. Y. Ledezma-Lozano, H. Chen, M. Vargas-Rojas, J. M. Salvador, I. V. Neagoe, R. Straub, M. Lopez-Santalla, K. Matsuo, H. Imaoka, J. Sieper, S. Ozaki, J. Bienvenu, H. Yu, H. Maeng, M. Fujimoto, A. Bucur, T. Nanki, Y. Matsuyama, R. Miyamoto, W. Maśliński, W. F. N. Chan, R. M. Goodfellow, C. Ferraro-Peyret, H. Bang, F. Batliwalla, M. Hoshino, K. Kaneko, S. Nomoto, R. S. Sadler, H. Yamada, S. Bae, M. Kosmač, K. Misaki, K. Sato, B. Diamond, B. L. Ferry, K. Otomo, F. Coury, A. R. Balanescu, T. Nishikawa, J. L. Nelson, N. Toplak, J. Kang, D. Zhang, F. Jones, C. Aranow, Y. Son, J. Ptacek, A. Komori, V. Cortez, N. van der Westhuizen, K. Onozaki, S. Tanaka, M. Steinbrich-Zöllner, P. K. Gregersen, H. Rangel-Villalobos, D. Chen, M. Inoue, M. Vázquez-Del Mercado, T. Hayashi, T. Kimata, U. Skalska, N. Eiró, S. Buranapraditkun, T. Hoshino, Y. Yu, Z. Newton, M. A. Llamas-Covarrubias, E. Bryl, H. Igarashi, M. Sawada, C. M. Chang, H. Tamemoto, A. Oyamada, Z. Rahman, F. Roncal, C. J. Calder, J. Rovensky, M. Herold, C. Martínez-A, J. F. Muñoz-Valle, E. C. Wang, K. Nakajima, J. Woo, S. Serada, T. Horita, D. Halbritter, Y. Akiyama, S. Minota, M. Tsuge, S. Yasuda, H. Huang, C. Probst, S. Itoh, S. Kumagai, T. Ito, C. A. Roberts, S. Capellino, J. Mulero, M. Yamasaki, T. Mori, N. Lai, H. Kim, M. Fleck, H. Oda, V. Čurin Šerbec, Y. Ozaki, S. Okamoto, R. Cimaz, S. Rome, J. Schölmerich, N. Jeerapadungkiat, T. Mimura, A. Tuchynova, L. Albulescu, R. Williams, P. Ammaranond, S. Sato, D. Goto, H. Yoshikawa, C. J. Atkins, G. Cioaca, C. Wong, M. Salvador-Bernaldez, K. Ishihara, V. Preoteasa, A. Daca, I. Ionita, E. Kontny, F. van Wijk, M. B. Hale, K. Yuge, Y. Sakazaki, E. J. Wehrens, and K. Migita

Subjects
Human studies, business.industry, Rheumatoid arthritis, Immunology, medicine, Immunology and Allergy, General Medicine, medicine.disease, business, Joint (geology)
Published
2010

5. AB0029 Relationship SCD36 Levels and Disease Activity in Patients with Rheumatoid Arthritis

Author

P.M. Madrigal Ruíz, A.A. Saldaña Millan, M Vázquez-Del Mercado, B.T. Martin Marquez, J.D.J.E. Gόmez Bañuelos, E. Chavarría Άvila, and R. E. Navarro Hernández

Subjects
medicine.medical_specialty, CD36, medicine.medical_treatment, Immunology, Inflammation, 030204 cardiovascular system & hematology, Gastroenterology, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, 0302 clinical medicine, Insulin resistance, Rheumatology, Internal medicine, medicine, Immunology and Allergy, Platelet activation, Scavenger receptor, biology, business.industry, Insulin, medicine.disease, 030220 oncology & carcinogenesis, Rheumatoid arthritis, biology.protein, medicine.symptom, business, Lipoprotein
Abstract

Background The main cause of death in RA patients is cardiovascular disease [1]. CD36 is a scavenger receptor has been postulated as a molecule involved in the atherogenic process [2,3]. A soluble fraction, sCD36 has been reported and has been proposed as a marker of atherosclerosis and other metabolic diseases [4,5], however, little is known of the pathways involved in these processes in RA. Objectives The objective of this study was to evaluate the levels of sCD36 and examine the association between clinical characteristics, disease activity and inflammatory markers in patients with RA. Methods The study groups were composed of 59 patients with RA (ACR/EULAR 2010) vs. 79 controls. sCD36, PCR, FR, Anti-CCP, insulin, TC, TG, HDL-C, VLDL-C, LDL-c were measured by ELISA. Index Disease Activity 28 (DAS-28) C-reactive protein (CRP) was calculated. VSG by Wintrobe method. cIMT using a Class B ultrasonography. Data were analyzed using descriptive statistics, Student t test, chi-square and ANOVA, as appropriate, with SPSS V.23 software. Results We found high levels of sCD36 in the control group (1861.10 ±6491.42±29.87 vs. 76.71, P Conclusions High levels of sCD36 were observed in serum from RA patients compared to a control group, as well as a relationship between sCD36 levels and Index Disease Activity 28 by pCr. It could be proposed to sCD36 as a marker of clinical activity of RA, however, more studies are needed to validate our findings and clarify the regulation and the role of sCD36 in RA. References Solomon, D.H., et al., Cardiovascular morbidity and mortality in women diagnosed with rheumatoid arthritis. Circulation, 2003. 107(9): p. 1303–7. Freeman, M.W., Scavenger receptors in atherosclerosis. Curr Opin Hematol, 1997. 4(1): p. 41–7. Silverstein, R.L., Inflammation, atherosclerosis, and arterial thrombosis: role of the scavenger receptor CD36. Cleve Clin J Med, 2009. 76 Suppl 2: p. S27–30. Handberg, A., et al., Identification of the oxidized low-density lipoprotein scavenger receptor CD36 in plasma: a novel marker of insulin resistance. Circulation, 2006. 114(11): p. 1169–76. Liani, R., et al., Plasma levels of soluble CD36, platelet activation, inflammation, and oxidative stress are increased in type 2 diabetic patients. Free Radic Biol Med, 2012. 52(8): p. 1318–24. Disclosure of Interest None declared

Published
2016

8. AB0120 Hearing Impairment and Tympano-Ossicular Compliance Are Affected by Disease Activity in Rheumatoid Arthritis

Author

M. Vázquez del Mercado Espinosa, B.T. Martin Marquez, J.D.J.E. Gόmez Bañuelos, C. Chavez Martin, R. E. Navarro Hernández, A.A. Saldaña Millan, and H. Macías Reyes

Subjects
medicine.medical_specialty, medicine.diagnostic_test, biology, business.industry, Immunology, C-reactive protein, Rheumatoid nodule, Tympanometry, Audiology, medicine.disease, General Biochemistry, Genetics and Molecular Biology, Disease activity, Rheumatology, Rheumatoid arthritis, Internal medicine, Erythrocyte sedimentation rate, medicine, biology.protein, Immunology and Allergy, Analysis of variance, medicine.symptom, Audiometry, business
Abstract

Background Both sensorineural hearing impairment (SNHI) and conductuve hearing impairment (CHI) have been reported in about 50% of patients with rheumatoid arthritis (RA). Previous reports have related SNHI with advanced age, disease activity, rheumatoid nodules, erythrocyte sedimentation rate (ESR), serum IL-6 and serum matrix metalloproteases. These findings are suggestive that inflammatory activitiy in RA may be related with SNHI development. Notwhitstanding, scarce information about the impairment of tympano-ossicular complex compliance is reported. Objectives The aim of this study is to evaluate hearing impairment (HI) in patients with RA and examined the association between clinical characteristics, disease activity and inflammatory markers in Mexican patients with RA. Methods The study group was comprised of 41 patients with RA. Patients were examined using pure-tone audiometry and tympanometry. The Disease Activity Index 28 (DAS-28) by c reactive protein (cRP) was calculated. Data was analyzed using descriptive statistics, Student9s T test, chi-square and ANOVA, accordingly with SPSS V.18 software. Results We found 58.5% RA patients with SNHI. Of these, 9.7% had superficial, 9.7% mild and 2.4% profound SNHI. Patients with SNHI were older at diagnosis than patients without SNHI (44.5±8.7 vs 32.1±10.1, P 5.1) vs. 17.6% of A tympanogram group (p vs. 0.67±0.33 vs. 0.50±0.18, P =0.01. Conclusions The type and degree most prevalent of HI in our study group was superficial SNHL and was found to be related with aging and older age at diagnosis. These findings suggest that ear involvement in RA, may exacerbate aging related HI Increasing disease activity. Levels of inflammatory markers and the presence of anti-CCP antibodies are related with worse HI in RA. Disclosure of Interest None declared

Published
2015

9. FRI0081 Titers of Anti-Ccp Antibodies, IL-6, Tnf-Alpha and CRP Are Associated with Increased Carotid Intima-Media Thickness: Cross-Sectional Analysis of A Rheumatoid Arthritis Group without Cardiovascular Risk Factors

Author

A.D. Rocha Muñoz, E.A. Martinez Garcia, M. Figueroa Sanchez, J. Andrade-Garduño, B T Martín-Márquez, R. E. Navarro Hernández, A.G. Bernard Medina, L. Nuñez Atahualpa, J. Aguilar Arreola, L. Gόnzalez Lόpez, Esperanza Lopez Gomez, M. Vazquez del Mercado, E. Corona Sanchez, A. Nuñez-Atahualpa, J. I. Gamez Nava, and R Vargas-Ramírez

Subjects
musculoskeletal diseases, medicine.medical_specialty, biology, business.industry, Immunology, Antibody titer, Disease, medicine.disease, Gastroenterology, General Biochemistry, Genetics and Molecular Biology, Pathogenesis, Rheumatology, Intima-media thickness, Internal medicine, Rheumatoid arthritis, Heart failure, medicine, biology.protein, Immunology and Allergy, Myocardial infarction, skin and connective tissue diseases, Interleukin 6, business
Abstract

Background The main causes of death in Rheumatoid Arthritis (RA) are cardiovascular events related to early atherosclerosis, myocardial infarction and congestive heart failure. The risk for cardiovascular disease it it not completely explained by the traditionally accepted cardiovascular risk factors. Inflammatory pathways of RA might be involved in the pathogenesis of subclinical atherosclerosis. Objectives To evaluate the relationship of anti-CCP antibody titers, serum IL-6, TNFa and high sensitivity c-Reactive Protein with increased carotid intima-media thickness (cIMT) in patients with RA without cardiovascular risk factors. Methods Sixty patients with RA, 27 anti-CCP positive and 33 anti-CCP negative, and 62 controls (HC) matched by age and gender. All groups were assessed for comorbidities, demographics, clinical evaluations, and cardiovascular risk calculated by atherogenic index of plasma (AIP). The cIMT was performed by high-resolution B-mode ultrasound by a single operator. Serum titers of anti-CCP, hs-cRP, levels of TNFα and IL-6 were measured by ELISA. Results The anti-CCP positive RA patients showed increased cIMT compared to HC and anti-CCP negative patients (p Conclusions High levels of anti-CCP and hs-cRP are useful markers of an increased cIMT and cardiovascular risk supporting a clinical role of the preventive measurement of cIMT in RA Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.5947

Published
2014

10. catA, a new Aspergillus nidulans gene encoding a developmentally regulated catalase

Author

R E, Navarro, M A, Stringer, W, Hansberg, W E, Timberlake, and J, Aguirre

Subjects
Base Sequence, Genes, Fungal, Molecular Sequence Data, Gene Expression Regulation, Developmental, Amino Acid Sequence, RNA, Messenger, Catalase, Aspergillus nidulans
Abstract

Aspergillus nidulans asexual sporulation (conidiation) is a model system for studying gene regulation and development. The CAN5 cDNA is one of several clones isolated based on transcript induction during conidiation. Here we present the molecular characterization of its corresponding gene, demonstrating that it encodes a developmentally regulated catalase, designated catA. The catA 744-amino-acid-residue polypeptide shows significant identity to other catalases. Its similarity to prokaryotic catalases is greater than to other fungal catalases. catA mRNA is barely detectable in growing mycelia, highly induced during sporulation, and present in isolated spores. However, catA expression is not dependent on the developmental regulatory genes brlA, abaA and wetA. Direct catalase activity determination in native gels revealed the existence of two bands of activity. One of these bands represented the major activity during vegetative growth and was induced during sporulation. The second catalase activity appeared after the induction of sporulation and was the predominant activity in spores. Disruption of catA abolished the major spore catalase without eliminating the vegetative activity, indicating the existence of at least two catalase genes in A. nidulans. catA-disrupted mutants produced spores that were sensitive to H2O2, as compared to wild-type spores. The increase in the activity of the vegetative catalase and the appearance of a second catalase during asexual sporulation is consistent with the occurrence of an oxidative stress during development.

Published
1996

11. Human genome meeting 2016

Author

Srivastava, A. K., Wang, Y., Huang, R., Skinner, C., Thompson, T., Pollard, L., Wood, T., Luo, F., Stevenson, R., Polimanti, R., Gelernter, J., Lin, X., Lim, I. Y., Wu, Y., Teh, A. L., Chen, L., Aris, I. M., Soh, S. E., Tint, M. T., MacIsaac, J. L., Yap, F., Kwek, K., Saw, S. M., Kobor, M. S., Meaney, M. J., Godfrey, K. M., Chong, Y. S., Holbrook, J. D., Lee, Y. S., Gluckman, P. D., Karnani, N., Kapoor, A., Lee, D., Chakravarti, A., Maercker, C., Graf, F., Boutros, M., Stamoulis, G., Santoni, F., Makrythanasis, P., Letourneau, A., Guipponi, M., Panousis, N., Garieri, M., Ribaux, P., Falconnet, E., Borel, C., Antonarakis, S. E., Kumar, S., Curran, J., Blangero, J., Chatterjee, S., Akiyama, J., Auer, D., Berrios, C., Pennacchio, L., Donti, T. R., Cappuccio, G., Miller, M., Atwal, P., Kennedy, A., Cardon, A., Bacino, C., Emrick, L., Hertecant, J., Baumer, F., Porter, B., Bainbridge, M., Bonnen, P., Graham, B., Sutton, R., Sun, Q., Elsea, S., Hu, Z., Wang, P., Zhu, Y., Zhao, J., Xiong, M., Bennett, David A., Hidalgo-Miranda, A., Romero-Cordoba, S., Rodriguez-Cuevas, S., Rebollar-Vega, R., Tagliabue, E., Iorio, M., D’Ippolito, E., Baroni, S., Kaczkowski, B., Tanaka, Y., Kawaji, H., Sandelin, A., Andersson, R., Itoh, M., Lassmann, T., Hayashizaki, Y., Carninci, P., Forrest, A. R. R., Semple, C. A., Rosenthal, E. A., Shirts, B., Amendola, L., Gallego, C., Horike-Pyne, M., Burt, A., Robertson, P., Beyers, P., Nefcy, C., Veenstra, D., Hisama, F., Bennett, R., Dorschner, M., Nickerson, D., Smith, J., Patterson, K., Crosslin, D., Nassir, R., Zubair, N., Harrison, T., Peters, U., Jarvik, G., Menghi, F., Inaki, K., Woo, X., Kumar, P., Grzeda, K., Malhotra, A., Kim, H., Ucar, D., Shreckengast, P., Karuturi, K., Keck, J., Chuang, J., Liu, E. T., Ji, B., Tyler, A., Ananda, G., Carter, G., Nikbakht, H., Montagne, M., Zeinieh, M., Harutyunyan, A., Mcconechy, M., Jabado, N., Lavigne, P., Majewski, J., Goldstein, J. B., Overman, M., Varadhachary, G., Shroff, R., Wolff, R., Javle, M., Futreal, A., Fogelman, D., Bravo, L., Fajardo, W., Gomez, H., Castaneda, C., Rolfo, C., Pinto, J. A., Akdemir, K. C., Chin, L., Patterson, S., Statz, C., Mockus, S., Nikolaev, S. N., Bonilla, X. I., Parmentier, L., King, B., Bezrukov, F., Kaya, G., Zoete, V., Seplyarskiy, V., Sharpe, H., McKee, T., Popadin, K., Basset-Seguin, N., Chaabene, R. Ben, Andrianova, M., Verdan, C., Grosdemange, K., Sumara, O., Eilers, M., Aifantis, I., Michielin, O., de Sauvage, F., Antonarakis, S., Likhitrattanapisal, S., Lincoln, S., Kurian, A., Desmond, A., Yang, S., Kobayashi, Y., Ford, J., Ellisen, L., Peters, T. L., Alvarez, K. R., Hollingsworth, E. F., Lopez-Terrada, D. H., Hastie, A., Dzakula, Z., Pang, A. W., Lam, E. T., Anantharaman, T., Saghbini, M., Cao, H., Gonzaga-Jauregui, C., Ma, L., King, A., Rosenzweig, E. Berman, Krishnan, U., Reid, J. G., Overton, J. D., Dewey, F., Chung, W. K., Small, K., DeLuca, A., Cremers, F., Lewis, R. A., Puech, V., Bakall, B., Silva-Garcia, R., Rohrschneider, K., Leys, M., Shaya, F. S., Stone, E., Sobreira, N. L., Schiettecatte, F., Ling, H., Pugh, E., Witmer, D., Hetrick, K., Zhang, P., Doheny, K., Valle, D., Hamosh, A., Jhangiani, S. N., Akdemir, Z. Coban, Bainbridge, M. N., Charng, W., Wiszniewski, W., Gambin, T., Karaca, E., Bayram, Y., Eldomery, M. K., Posey, J., Doddapaneni, H., Hu, J., Sutton, V. R., Muzny, D. M., Boerwinkle, E. A., Lupski, J. R., Gibbs, R. A., Shekar, S., Salerno, W., English, A., Mangubat, A., Bruestle, J., Thorogood, A., Knoppers, B. M., Takahashi, H., Nitta, K. R., Kozhuharova, A., Suzuki, A. M., Sharma, H., Cotella, D., Santoro, C., Zucchelli, S., Gustincich, S., Mulvihill, J. J., Baynam, G., Gahl, W., Groft, S. C., Kosaki, K., Lasko, P., Melegh, B., Taruscio, D., Ghosh, R., Plon, S., Scherer, S., Qin, X., Sanghvi, R., Walker, K., Chiang, T., Muzny, D., Wang, L., Black, J., Boerwinkle, E., Weinshilboum, R., Gibbs, R., Karpinets, T., Calderone, T., Wani, K., Yu, X., Creasy, C., Haymaker, C., Forget, M., Nanda, V., Roszik, J., Wargo, J., Haydu, L., Song, X., Lazar, A., Gershenwald, J., Davies, M., Bernatchez, C., Zhang, J., Woodman, S., Chesler, E. J., Reynolds, T., Bubier, J. A., Phillips, C., Langston, M. A., Baker, E. J., Lin, N., Amos, C., Calhoun, V., Dobretsberger, O., Egger, M., Leimgruber, F., Sadedin, S., Oshlack, A., Antonio, V. A. A., Ono, N., Ahmed, Z., Bolisetty, M., Zeeshan, S., Anguiano, E., Sarkar, A., Nandineni, M. R., Zeng, C., Shao, J., Liang, T., Pham, K., Chee-Wei, Y., Dongsheng, L., Lai-Ping, W., Lian, D., Hee, R. O. Twee, Yunus, Y., Aghakhanian, F., Mokhtar, S. S., Lok-Yung, C. V., Bhak, J., Phipps, M., Shuhua, X., Yik-Ying, T., Kumar, V., Boon-Peng, H., Campbell, I., Young, M. -A., James, P., Rain, M., Mohammad, G., Kukreti, R., Pasha, Q., Akilzhanova, A. R., Guelly, C., Abilova, Z., Rakhimova, S., Akhmetova, A., Kairov, U., Trajanoski, S., Zhumadilov, Z., Bekbossynova, M., Schumacher, C., Sandhu, S., Harkins, T., Makarov, V., Glenn, R., Momin, Z., Dilrukshi, B., Chao, H., Meng, Q., Gudenkauf, B., Kshitij, R., Jayaseelan, J., Nessner, C., Lee, S., Blankenberg, K., Lewis, L., Han, Y., Dinh, H., Jireh, S., Buhay, C., Liu, X., Wang, Q., Ding, Y., Veeraraghavan, N., Yang, Y., Beaudet, A. L., Eng, C. M., Worley, K. C. C., Liu, Y., Hughes, D. S. T., Murali, S. C., Harris, R. A., English, A. C., Hampton, O. A., Larsen, P., Beck, C., Wang, M., Kovar, C. L., Salerno, W. J., Yoder, A., Richards, S., Rogers, J., Raveenedran, M., Xue, C., Dahdouli, M., Cox, L., Fan, G., Ferguson, B., Hovarth, J., Johnson, Z., Kanthaswamy, S., Kubisch, M., Platt, M., Smith, D., Vallender, E., Wiseman, R., Below, J., Yu, F., Lin, J., Zhang, Y., Ouyang, Z., Moore, A., Wang, Z., Hofmann, J., Purdue, M., Stolzenberg-Solomon, R., Weinstein, S., Albanes, D., Liu, C. 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