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Journal articles on the topic 'Mice – Embryology'

To see the other types of publications on this topic, follow the link: Mice – Embryology.

Author: Grafiati

Published: 4 June 2021

Last updated: 29 January 2023

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1

Salvadori, Maria Letícia Baptista, Thais Borges Lessa, Fabiele Baldino Russo, Renata Avancini Fernandes, José Roberto Kfoury, Patricia Cristina Baleeiro Beltrão Braga, and Maria Angélica Miglino. "Mice embryology: A microscopic overview." Microscopy Research and Technique 75, no. 10 (June 22, 2012): 1437–44. http://dx.doi.org/10.1002/jemt.22087.

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2

Martins, José Luiz, Maurício Macedo, and Edna Frasson de Souza Montero. "Anorectal Malformation: State of the Art in Translating Experimental Research to the Bedside." European Journal of Pediatric Surgery 29, no. 04 (August 2019): 368–70. http://dx.doi.org/10.1055/s-0039-1694743.

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AbstractThe embryology of anorectal malformation (ARM) is a controversial issue. The study in humans is difficult due to the scarcity of fetuses with this anomaly. Therefore, ARM animal models, naturally obtained or induced by drugs, have been employed to understand physiopathology and possible treatments. Pigs, rabbits, rats, and mice have been employed as animal models. Additionally, many drugs have been used with this purpose: Etretinate, Ethylenethiourea, and Adriamycin. The animal more frequently used is the rat because of good reproducibility, low cost, and easy handling. Pig is a good model, but it is expensive, and difficult to handling and lodging. Concerning the drugs, Adriamycin promotes a more severe ARM compared with Ethylenethiourea. The models of ARM are of value in the understanding of the embryologic development. Nowadays, researches are aimed at identifying the molecular mechanism of this process, providing the basis for the application of tissue engineering in future experiments with ARM.

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3

Helppi, Jussi, Ronald Naumann, and Oliver Zierau. "Phytoestrogen-containing diets offer benefits for mouse embryology but lead to fewer offspring being produced." Laboratory Animals 54, no. 6 (February 12, 2020): 536–45. http://dx.doi.org/10.1177/0023677219898486.

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One of the most commonly used protein sources in rodent diets is soy, which is naturally rich in phytoestrogens. Although phytoestrogens have shown potential health benefits in humans, they may also have the ability to disrupt reproduction. Consequently, there has been a tendency to try to exclude them from rodent diets. In the current study, we investigated whether phytoestrogen content in the mouse diet could affect reproduction in mice used as embryo donors. Donor mice (C57BL/6JOlaHsd) were maintained with three different diets: high phytoestrogen (ca. 400 mg/kg genistein), low phytoestrogen (ca. 10 mg/kg genistein) and standard breeding diet (ca. 120 mg/kg genistein). Mice fed a high phytoestrogen diet had a high yield of plugs, embryos, and injectable embryos, as well as producing good quality embryos. Results from donor mice fed a low phytoestrogen diet were consistently but only slightly inferior, whereas mice fed a standard diet performed the poorest. Interestingly, the largest number of born and weaned offspring were observed when recipient females received embryos from the standard diet group. Sperm yield and quality of stud males did not differ between the groups. We surmize that for experimental endpoints requiring fertilized embryos it may be more beneficial to feed mice a diet containing phytoestrogen, but if the goal is to produce transgenic mice, a diet high in phytoestrogen may be inadvisable. In conclusion, care should be taken when selecting a diet for experimental mouse colonies as phytoestrogen could influence the study outcome.

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4

Godin, Isabelle, and Ana Cumano. "Of birds and mice: hematopoietic stem cell development." International Journal of Developmental Biology 49, no. 2-3 (2005): 251–57. http://dx.doi.org/10.1387/ijdb.041945ig.

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5

Song, Haichen, Yu Xu, Wenchuan Chang, Junli Zhuang, and Xiaowei Wu. "Negative pressure wound therapy promotes wound healing by suppressing macrophage inflammation in diabetic ulcers." Regenerative Medicine 15, no. 12 (December 2020): 2341–49. http://dx.doi.org/10.2217/rme-2020-0050.

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Aim: This work aims to explore the biological role of negative pressure wound therapy (NPWT) in the treatment of diabetic ulcer. Materials & methods: Full-thickness skin defects were created in diabetic (db/db) and non diabetic (db/m) mice to create wound models. The mice were received NPWT or rapamycin injection. Mouse macrophage cells (Raw264.7) were treated with lipopolysaccharide to induce inflammatory response, and then received negative pressure treatment. We observed the wound healing of mice and examined gene and protein expression and CD68+ macrophage levels. Results: NPWT notably enhanced the wound closure ratio, and inhibited the LC3-II/LC3-I ratio and Beclin-1 expression in diabetes mellitus (DM) mice. NPWT decreased CD68+ macrophage levels in wound tissues of DM mice. The influence conferred by NPWT was abolished by rapamycin treatment. Negative pressure repressed the LC3-II/LC3-I ratio and the expression of Beclin-1, TNF-α, IL-6 and IL-1β in the Raw264.7 cells. Conclusion: NPWT promotes wound healing by suppressing autophagy and macrophage inflammation in DM.

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6

Nakajima, Mitsunari, Shigeki Yuasa, Masaya Ueno, Nobuyuki Takakura, Haruhiko Koseki, and Takuji Shirasawa. "Abnormal blood vessel development in mice lacking presenilin-1." Mechanisms of Development 120, no. 6 (June 2003): 657–67. http://dx.doi.org/10.1016/s0925-4773(03)00064-9.

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7

Anzai, Hiroko, Akihide Kamiya, Haruki Shirato, Takashi Takeuchi, and Atsushi Miyajima. "Impaired differentiation of fetal hepatocytes in homozygous jumonji mice." Mechanisms of Development 120, no. 7 (July 2003): 791–800. http://dx.doi.org/10.1016/s0925-4773(03)00071-6.

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8

Walker, Kenneth, Georgina Caruana, Sunder Sims-Lucas, Mai Sarraj, John Bertram, and Kaye Stenvers. "06-P014 High nephron number in betaglycan heterozygous mice." Mechanisms of Development 126 (August 2009): S124. http://dx.doi.org/10.1016/j.mod.2009.06.240.

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9

Simpson, Kaylene J. "MMTV-trBrca1 mice display strain-dependent abnormalities in vaginal development." International Journal of Developmental Biology 48, no. 7 (2004): 675–78. http://dx.doi.org/10.1387/ijdb.041849ks.

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10

Tamura, Shinobu, Yoshihiro Morikawa, Minoru Tanaka, Atsushi Miyajima, and Emiko Senba. "Developmental expression pattern of oncostatin M receptor β in mice." Mechanisms of Development 115, no. 1-2 (July 2002): 127–31. http://dx.doi.org/10.1016/s0925-4773(02)00081-3.

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11

Schimmang, Thomas, Gonzalo Alyarez-Bolado, Liliana Minichiello, Esther Vazquez, Fernando Giraldez, Rüdiger Klein, and Juan Represa. "Survival of inner ear sensory neurons in trk mutant mice." Mechanisms of Development 64, no. 1-2 (June 1997): 77–85. http://dx.doi.org/10.1016/s0925-4773(97)00047-6.

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12

Perez, Ana V., Michael Perrine, Nicolas Brainard, and Kathryn G. Vogel. "Scleraxis (Scx) directs lacZ expression in tendon of transgenic mice." Mechanisms of Development 120, no. 10 (October 2003): 1153–63. http://dx.doi.org/10.1016/j.mod.2003.08.003.

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13

Morrison, Alastair, Chitrita Chaudhuri, Linda Ariza-McNaughton, Ian Muchamore, Atsushi Kuroiwa, and Robb Krumlauf. "Comparative analysis of chicken Hoxb-4 regulation in transgenic mice." Mechanisms of Development 53, no. 1 (September 1995): 47–59. http://dx.doi.org/10.1016/0925-4773(95)00423-8.

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14

Ruetten, Hannah, Kyle A. Wegner, Helen L. Zhang, Peiqing Wang, Jaskiran Sandhu, Simran Sandhu, Jacquelyn Morkrid, et al. "Insight and Resources From a Study of the “Impact of Sex, Androgens, and Prostate Size on C57BL/6J Mouse Urinary Physiology." Toxicologic Pathology 47, no. 8 (October 29, 2019): 1038–42. http://dx.doi.org/10.1177/0192623319877867.

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The purpose of this symposium report is to summarize information from a session 3 oral presentation at the Society of Toxicologic Pathology Annual Symposium in Raleigh, North Carolina. Mice are genetically tractable and are likely to play an important role in elucidating environmental, genetic, and aging-related mechanisms of urinary dysfunction in men. We and others have made significant strides in developing quantitative methods for assessing mouse urinary function and our collaborators recently showed that aging male mice, like men, develop urinary dysfunction. Yet, it remains unclear how mouse prostate anatomy and histology relate to urinary function. The purpose of this report is to share foundational resources for evaluating mouse prostate histology and urinary physiology from our recent publication “Impact of Sex, Androgens, and Prostate Size on C57BL/6J Mouse Urinary Physiology: Functional Assessment.” We will begin with a review of prostatic embryology in men and mice, then move to comparative histology resources, and conclude with quantitative measures of rodent urinary physiology.

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15

Niu, Qiannan, Shuning Shen, Jiaojiao He, and Lei Wang. "CKIP-1 contributes to osteogenic differentiation of mouse bone marrow mesenchymal stem cells." Regenerative Medicine 16, no. 9 (September 2021): 847–59. http://dx.doi.org/10.2217/rme-2020-0119.

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Background: Osteogenesis greatly depends on the differentiation of bone marrow mesenchymal stem cells (BMSCs). CKIP-1 is considered to be a negative regulator of BMSCs. Methods: We established a CKIP-1 knockout mouse model, then isolated and cultured BMSCs from wild-type and knockout groups. Results: Our data demonstrated that CKIP-1 knockout significantly increased bone structure in the experimental mouse model and enhanced BMSC proliferation. CKIP-1 knockout contributed to osteoblastic and adipogenic differentiation. Furthermore, CKIP-1 regulated osteogenesis in BMSCs via the MAPK signaling pathway, and BMSCs from the CKIP-1 knockout mice were effective in repairing the skull defect null mice. Conclusion: Our results concluded that silencing of CKIP-1 promoted osteogenesis in experimental mice and increased BMSCs differentiation via upregulation of the MAPK signaling pathway.

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16

Gabriel, George C., Hisato Yagi, Xinxiu Xu, and Cecilia W. Lo. "Novel Insights into the Etiology, Genetics, and Embryology of Hypoplastic Left Heart Syndrome." World Journal for Pediatric and Congenital Heart Surgery 13, no. 5 (September 2022): 565–70. http://dx.doi.org/10.1177/21501351221102961.

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Hypoplastic left heart syndrome (HLHS) is a relatively rare severe congenital heart defect (CHD) closely linked to other left ventricular outflow tract (LVOT) lesions including bicuspid aortic valve (BAV), one of the most common heart defects. While HLHS, BAV, and other LVOT lesions have a strong genetic underpinning, their genetic etiology remains poorly understood. Findings from a large-scale mouse mutagenesis screen showed HLHS has a multigenic etiology and is genetically heterogenous, explaining difficulties in identifying the genetic causes of HLHS. In Ohia mice, HLHS shows incomplete penetrance. Some mice exhibited small LV with normal aorta, and others a normal LV with hypoplastic aorta, indicating the LV hypoplasia is not hemodynamically driven. In Ohia mutants, HLHS was found to have a digenic modular construction, with mutation in a chromatin modifier causing the small LV phenotype and mutation in Pcdha9 causing the aorta/aortic valve hypoplasia. The Pcdha9 mutation alone can cause BAV, and in the human genome two common deletion copy number variants spanning PCDHA7-10 are associated with BAV. Hence the digenic etiology of HLHS can account for the close association of HLHS, a rare CHD, with BAV, one of the most common CHD. Functional analysis of Ohia HLHS heart tissue showed severe mitochondrial dysfunction in the small LV, while the normal size RV is also affected but milder, suggesting possible role in vulnerability of surgically palliated HLHS patients to heart failure. These findings suggest insights into the genetics of HLHS may yield new therapies for improving outcome for patients with HLHS.

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17

Sugarman, Jeremy, and Debra JH Mathews. "Of mice and men: skin cells, stem cells and ethical uncertainties." Regenerative Medicine 4, no. 6 (November 2009): 791. http://dx.doi.org/10.2217/rme.09.65.

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18

Kraus, Petra, Diego Fraidenraich, and Cynthia A. Loomis. "Some distal limb structures develop in mice lacking Sonic hedgehog signaling." Mechanisms of Development 100, no. 1 (January 2001): 45–58. http://dx.doi.org/10.1016/s0925-4773(00)00492-5.

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19

Gründer, Albert, Thorsten T. Ebel, Moisés Mallo, Georg Schwarzkopf, Takehiko Shimizu, Albrecht E. Sippel, and Heinrich Schrewe. "Nuclear factor I-B (Nfib) deficient mice have severe lung hypoplasia." Mechanisms of Development 112, no. 1-2 (March 2002): 69–77. http://dx.doi.org/10.1016/s0925-4773(01)00640-2.

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20

Choi, Min-A., Wern-Joo Sohn, Hye-In Jung, Hong-In Shin, Sang Gyu Lee, Han-Sung Jung, and Jae-Young Kim. "03-P103 Morphogenesis and cellular mechanisms in mice molar root development." Mechanisms of Development 126 (August 2009): S97. http://dx.doi.org/10.1016/j.mod.2009.06.156.

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21

An, Seo-Young, Ye-Ji Lee, Sanjiv Neupane, Jong-Hwa Jun, Ji-Youn Kim, Youngkyun Lee, Karp-Shik Choi, et al. "Effects of vascular formation during alveolar bone process morphogenesis in mice." Mechanisms of Development 145 (July 2017): S151. http://dx.doi.org/10.1016/j.mod.2017.04.426.

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22

Reynolds, Kay, Eva Mezey, and Andreas Zimmer. "Activity of the β-retinoic acid receptor promoter in transgenic mice." Mechanisms of Development 36, no. 1-2 (December 1991): 15–29. http://dx.doi.org/10.1016/0925-4773(91)90068-h.

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23

Golas, Aniela, Anna Dzieza, Katarzyna Kuzniarz, and Jozefa Styrna. "Gene mapping of sperm quality parameters in recombinant inbred strains of mice." International Journal of Developmental Biology 52, no. 2-3 (2008): 287–93. http://dx.doi.org/10.1387/ijdb.072333ag.

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24

Hadjantonakis, Anna-Katerina, Marina Gertsenstein, Masahito Ikawa, Masaru Okabe, and Andras Nagy. "Generating green fluorescent mice by germline transmission of green fluorescent ES cells." Mechanisms of Development 76, no. 1-2 (August 1998): 79–90. http://dx.doi.org/10.1016/s0925-4773(98)00093-8.

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25

Yu, Hsiao-Man Ivy, Bo Liu, Frank Costantini, and Wei Hsu. "Impaired neural development caused by inducible expression of Axin in transgenic mice." Mechanisms of Development 124, no. 2 (February 2007): 146–56. http://dx.doi.org/10.1016/j.mod.2006.10.002.

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26

Ikeya, Makoto, Tetsuya Nosaka, Kumi Fukushima, Masako Kawada, Yasuhide Furuta, Toshio Kitamura, and Yoshiki Sasai. "Twisted gastrulation mutation suppresses skeletal defect phenotypes in Crossveinless 2 mutant mice." Mechanisms of Development 125, no. 9-10 (September 2008): 832–42. http://dx.doi.org/10.1016/j.mod.2008.06.011.

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27

Herrmann, David, Shuofei Cheng, Katrin Driller, Juha Partanen, and Annette Neubüser. "09-P054 Analysis of facial and palatal defects in Fgfr1 mutant mice." Mechanisms of Development 126 (August 2009): S166. http://dx.doi.org/10.1016/j.mod.2009.06.384.

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28

Ito, Ayako, Youhei Shinmyo, Masahiro Yamaguchi, Rika nakayama, Naoko Oshima, Hideaki Tanaka, and Ohta kunimasa. "12-P006 Analysis of morphological phenotypes in Tsukushi (TSK) KO mice brain." Mechanisms of Development 126 (August 2009): S190. http://dx.doi.org/10.1016/j.mod.2009.06.460.

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29

Mommaerts, Hendrik, Frank P. Luyten, and Przemko Tylzanowski. "21-P026 Molecular analysis of the muscle phenotype of Noggin null mice." Mechanisms of Development 126 (August 2009): S321. http://dx.doi.org/10.1016/j.mod.2009.06.891.

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30

Grzmil, Pawel, Zanabazar Enkhbaatar, Batjargal Gundsambuu, Odgerel Oidovsambuu, Safak Yalcin, Stephan Wolf, Wolfgang Engel, and Jrgen Neesen. "Early embryonic lethality in gene trap mice with disruption of the Arfgef2 gene." International Journal of Developmental Biology 54, no. 8-9 (2010): 1259–66. http://dx.doi.org/10.1387/ijdb.092959pg.

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31

Andres, Anne-Catherine, Nadia Munarini, Valentin Djonov, Salomé Bruneau, Gisela Zuercher, Saemi Loercher, Valeria Rohrbach, and Andrew Ziemiecki. "EphB4 receptor tyrosine kinase transgenic mice develop glomerulopathies reminiscent of aglomerular vascular shunts." Mechanisms of Development 120, no. 4 (April 2003): 511–16. http://dx.doi.org/10.1016/s0925-4773(02)00461-6.

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32

Wang, Zhao-Qi, Friedemann Kiefer, Pavel Urbánek, and Erwin F. Wagner. "Generation of completely embryonic stem cell-derived mutant mice using tetraploid blastocyst injection." Mechanisms of Development 62, no. 2 (March 1997): 137–45. http://dx.doi.org/10.1016/s0925-4773(97)00655-2.

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33

Troy, Tammy-Claire, Ramtin Rahbar, Azadeh Arabzadeh, Robert Man-Kit Cheung, and Kursad Turksen. "Delayed epidermal permeability barrier formation and hair follicle aberrations in Inv-Cldn6 mice." Mechanisms of Development 122, no. 6 (June 2005): 805–19. http://dx.doi.org/10.1016/j.mod.2005.03.001.

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34

Schild, Andreas, Stefan Isenmann, Naoyuki Tanimoto, Felix Tonagel, Mathias W. Seeliger, Lars M. Ittner, Alexandra Kretz, Egon Ogris, and Jürgen Götz. "Impaired development of the Harderian gland in mutant protein phosphatase 2A transgenic mice." Mechanisms of Development 123, no. 5 (May 2006): 362–71. http://dx.doi.org/10.1016/j.mod.2006.03.003.

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35

Chau, You-Ying, Kay Samuel, David Brownstein, David Dow, Joan Slight, Martin Waterfall, Elisabeth Freyer, and Nicholas Hastie. "03-P062 Wt1 is required for haematopoiesis in adult mice but not fetal." Mechanisms of Development 126 (August 2009): S84—S85. http://dx.doi.org/10.1016/j.mod.2009.06.115.

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36

McLain, Kersten, Claire Schreiner, Karen L. Yager, Jeffrey L. Stock, and S. Steven Potter. "Ectopic expression of Hox-2.3 induces craniofacial and skeletal malformations in transgenic mice." Mechanisms of Development 39, no. 1-2 (November 1992): 3–16. http://dx.doi.org/10.1016/0925-4773(92)90021-b.

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37

Püschel, Andreas W., Monte Westerfield, and Gregory R. Dressler. "Comparative analysis of Pax-2 protein distributions during neurulation in mice and zebrafish." Mechanisms of Development 38, no. 3 (September 1992): 197–208. http://dx.doi.org/10.1016/0925-4773(92)90053-m.

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38

Schrewe, Heinrich, Maureen Gendron-Maguire, Margaret L. Harbison, and Thomas Gridley. "Mice homozygous for a null mutation of activin βB are viable and fertile." Mechanisms of Development 47, no. 1 (July 1994): 43–51. http://dx.doi.org/10.1016/0925-4773(94)90094-9.

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39

Yasen, Aimaiti, Wending Li, Yusufukadier Maimaitinijiati, Abudusalamu Aini, Bo Ran, Hui Wang, Tuerhongjiang Tuxun, Yingmei Shao, Tuerganaili Aji, and Hao Wen. "Direct effects of transforming growth factor-β1 signaling on the differentiation fate of fetal hepatic progenitor cells." Regenerative Medicine 15, no. 6 (June 2020): 1719–33. http://dx.doi.org/10.2217/rme-2020-0002.

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Aim: To investigate direct roles of TGF-β1 signaling in the differentiation process of fetal hepatic progenitor cells (HPCs). Materials & methods: Exogenous TGF-β1 and SB431542 were added into fetal HPCs. Then, SB431542 was intraperitoneally injected into pregnant mice for 8 days. Results: Fetal HPCs treated with TGF-β1 differentiated into cholangiocytes. However, hepatocyte marker was highly expressed after inhibiting TGF-β1 signaling. In vivo, hematopoietic cells were gradually replaced with liver cells and TGF-β1 expression was evidently decreased as fetal liver developed. Inhibition of TGF-β1 signaling caused increase of ALB+ cells, but CK19 expression was more obvious in control mice livers. Conclusion: TGF-β1 signaling may play decisive roles in fetal HPCs differentiation into functional hepatocytes or cholangiocytes.

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40

Wilson, Doris B., and Darlene P. Wyatt. "Axial interactions during neurogenesis in dysraphic mice." Anatomy and Embryology 180, no. 5 (October 1989): 515–19. http://dx.doi.org/10.1007/bf00305127.

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41

Archacka, Karolina, Anna Ajduk, Pawel Pomorski, Katarzyna Szczepanska, Marek Maleszewski, and Maria A. Ciemerych. "Defective calcium release during in vitro fertilization of maturing oocytes of LT/Sv mice." International Journal of Developmental Biology 52, no. 7 (2008): 903–12. http://dx.doi.org/10.1387/ijdb.072397ka.

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42

Laissue, Paul, Gaetan Burgio, David l'Hote, Gilles Renault, Carmen Marchiol-Fournigault, Didier Fradelizi, Marc Fellous, et al. "Identification of Quantitative Trait Loci responsible for embryonic lethality in mice assessed by ultrasonography." International Journal of Developmental Biology 53, no. 4 (2009): 623–29. http://dx.doi.org/10.1387/ijdb.082613pl.

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43

Golas, Aniela, Paulina Malek, Malgorzata Piasecka, and Jozefa Styrna. "Sperm mitochondria diaphorase activity a gene mapping study of recombinant inbred strains of mice." International Journal of Developmental Biology 54, no. 4 (2010): 667–73. http://dx.doi.org/10.1387/ijdb.082778ag.

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44

Guzzo, Rosa M., Viktoria Andreeva, Douglas B. Spicer, and M. Hicham Drissi. "Persistent expression of Twist1 in chondrocytes causes growth plate abnormalities and dwarfism in mice." International Journal of Developmental Biology 55, no. 6 (2011): 641–47. http://dx.doi.org/10.1387/ijdb.103274rg.

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45

Liu, Jianmin, Lei Zhang, Dongmei Wang, Huaming Shen, Min Jiang, Pinchao Mei, Patrick S. Hayden, John R. Sedor, and Huaiyu Hu. "Congenital diaphragmatic hernia, kidney agenesis and cardiac defects associated with Slit3-deficiency in mice." Mechanisms of Development 120, no. 9 (September 2003): 1059–70. http://dx.doi.org/10.1016/s0925-4773(03)00161-8.

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46

Hidalgo, Alicia, and Charles ffrench-Constant. "The control of cell number during central nervous system development in flies and mice." Mechanisms of Development 120, no. 11 (November 2003): 1311–25. http://dx.doi.org/10.1016/j.mod.2003.06.004.

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47

Babbs, Christian, Helen Stewart, Louise Williams, Lyndsey Connell, Anne Goriely, Stephen Twigg, Kim Smith, Tracey Lester, and Andrew Wilkie. "06-P003 Imbalance in ephrin-b1 expression leads to hypertelorism in humans and mice." Mechanisms of Development 126 (August 2009): S120—S121. http://dx.doi.org/10.1016/j.mod.2009.06.229.

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48

Masami, Kanai-Azuma, Yuichiro Miura, Mami Uemura, Hayato Kawakami, and Yoshiakira Kanai. "06-P012 Haploinsufficiency of Sox17 causes defective maturation of fetal livers in C57BL6 mice." Mechanisms of Development 126 (August 2009): S123—S124. http://dx.doi.org/10.1016/j.mod.2009.06.238.

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49

Sierig, Ralph, Dagmar Kruspe, Jürgen Kastner, Claudia Lück, Ralph Witzgall, and Christoph Englert. "09-P005 The Wilms tumour protein is required for kidney function in adult mice." Mechanisms of Development 126 (August 2009): S152. http://dx.doi.org/10.1016/j.mod.2009.06.335.

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50

Sagnol, Sébastien, Laurette Morlé, Aouatef Ait-Lounis, Walter Reith, and Bénédicte Durand. "16-P006 The ciliogenic transcription factor RFX3 is required for lung development in mice." Mechanisms of Development 126 (August 2009): S263—S264. http://dx.doi.org/10.1016/j.mod.2009.06.697.

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