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Journal articles on the topic 'Tissue-specific knockout'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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1

Burns, Kathleen H., Julio E. Agno, Piotr Sicinski та Martin M. Matzuk. "Cyclin D2 and p27 Are Tissue-Specific Regulators of Tumorigenesis in Inhibin α Knockout Mice". Molecular Endocrinology 17, № 10 (2003): 2053–69. http://dx.doi.org/10.1210/me.2003-0038.

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Abstract Inhibins are heterodimeric (α:βA and α:βB) endocrine, paracrine, and autocrine factors of the TGFβ superfamily that are produced predominantly by ovarian granulosa cells in females and testicular Sertoli cells in males. Control of granulosa and Sertoli cell proliferation is lost in the inhibin α (Inhα) knockout mouse model, leading to gonadotropin-dependent gonadal tumors of the granulosa/Sertoli cell lineage in both females and males. Castrate Inhα knockout mice develop sex steroidogenic tumors of the adrenal cortex. Physiological control of granulosa/Sertoli cell cycle progression d

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2

Mirandola, Sandra R., Alexei P. Kudin, and Wolfram S. Kunz. "Tissue specific effects of MnSOD knockout in mice." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1797 (July 2010): 61. http://dx.doi.org/10.1016/j.bbabio.2010.04.199.

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3

Bagnall, Dr Alan, David Webb, and Dr Yuri Kotelevtsev. "Tissue Specific Knockout of the Mouse Endothelin B receptor." Clinical Science 103, s47 (2002): 15P. http://dx.doi.org/10.1042/cs103015p.

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4

de Lange, Willem J., Carmen M. Halabi, Andreas M. Beyer, and Curt D. Sigmund. "Germ line activation of the Tie2 and SMMHC promoters causes noncell-specific deletion of floxed alleles." Physiological Genomics 35, no. 1 (2008): 1–4. http://dx.doi.org/10.1152/physiolgenomics.90284.2008.

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Tissue-specific knockouts generated through Cre-loxP recombination have become an important tool to manipulate the mouse genome. Normally, two successive rounds of breeding are performed to generate mice carrying two floxed target-gene alleles and a transgene expressing Cre-recombinase tissue-specifically. We show herein that two promoters commonly used to generate endothelium-specific ( Tie2) and smooth muscle-specific [smooth muscle myosin heavy chain ( Smmhc)] knockout mice exhibit activity in the female and male germ lines, respectively. This can result in the inheritance of a null allele

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5

Wei, C., A. Rashid, C. Amos, M. Gannon, and M. L. Frazier. "LKB1 GENE TISSUE SPECIFIC KNOCKOUT MOUSE MODEL FOR PANCREATIC CANCER." Pancreas 31, no. 4 (2005): 478. http://dx.doi.org/10.1097/01.mpa.0000193795.44003.bb.

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6

Kos, Claudine H. "Cre/loxP System for Generating Tissue-specific Knockout Mouse Models." Nutrition Reviews 62, no. 6 (2004): 243–46. http://dx.doi.org/10.1301/nr2004.jun243-246.

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7

Sakai, Satoshi. "Development of Tissue- and Time-specific Gene Knockout in Mice." Journal of Cardiac Failure 13, no. 6 (2007): S10. http://dx.doi.org/10.1016/j.cardfail.2007.06.042.

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8

Zhang, Cong, Kalyne Bertolin, Raj Duggavathi, and Bruce D. Murphy. "Orphan Nuclear Receptors in Reproduction: Lessons from Tissue-Specific Knockout Mice." Biology of Reproduction 85, Suppl_1 (2011): 161. http://dx.doi.org/10.1093/biolreprod/85.s1.161.

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9

Rindler, Tara N., Valerie M. Lasko, Michelle L. Nieman, Motoi Okada, John N. Lorenz та Jerry B. Lingrel. "Knockout of the Na,K-ATPase α2-isoform in cardiac myocytes delays pressure overload-induced cardiac dysfunction". American Journal of Physiology-Heart and Circulatory Physiology 304, № 8 (2013): H1147—H1158. http://dx.doi.org/10.1152/ajpheart.00594.2012.

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The α2-isoform of the Na,K-ATPase (α2) is the minor isoform of the Na,K-ATPase expressed in the cardiovascular system and is thought to play a critical role in the regulation of cardiovascular hemodynamics. However, the organ system/cell type expressing α2 that is required for this regulation has not been fully defined. The present study uses a heart-specific knockout of α2 to further define the tissue-specific role of α2 in the regulation of cardiovascular hemodynamics. To accomplish this, we developed a mouse model using the Cre/loxP system to generate a tissue-specific knockout of α2 in the

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10

Yamada, Atsushi, Atsu Aiba, and Ryutaro Kamijo. "Rho family small G proteins: Lessons from tissue-specific gene knockout studies." Journal of Oral Biosciences 56, no. 1 (2014): 23–29. http://dx.doi.org/10.1016/j.job.2013.10.003.

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11

Ludwig, Thomas, Peter Fisher, Vundavalli Murty, and Argiris Efstratiadis. "Development of mammary adenocarcinomas by tissue-specific knockout of Brca2 in mice." Oncogene 20, no. 30 (2001): 3937–48. http://dx.doi.org/10.1038/sj.onc.1204512.

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12

Li, H., J. Wang, H. Wilhelmsson, et al. "Genetic modification of survival in tissue-specific knockout mice with mitochondrial cardiomyopathy." Proceedings of the National Academy of Sciences 97, no. 7 (2000): 3467–72. http://dx.doi.org/10.1073/pnas.97.7.3467.

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13

Softic, Samir, Jeremie Boucher, Marie H. Solheim, et al. "Lipodystrophy Due to Adipose Tissue–Specific Insulin Receptor Knockout Results in Progressive NAFLD." Diabetes 65, no. 8 (2016): 2187–200. http://dx.doi.org/10.2337/db16-0213.

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14

Qian, Shinguang, Fumin Fu, Wei Li, Qi Chen, and Frederic J. de Sauvage. "Primary Role of the Liver in Thrombopoietin Production Shown by Tissue-Specific Knockout." Blood 92, no. 6 (1998): 2189–91. http://dx.doi.org/10.1182/blood.v92.6.2189.

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15

Whirledge, Shannon, and Donald B. DeFranco. "Glucocorticoid Signaling in Health and Disease: Insights From Tissue-Specific GR Knockout Mice." Endocrinology 159, no. 1 (2017): 46–64. http://dx.doi.org/10.1210/en.2017-00728.

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16

Guerra, Carmen, Paloma Navarro, Angela M. Valverde, et al. "Brown adipose tissue–specific insulin receptor knockout shows diabetic phenotype without insulin resistance." Journal of Clinical Investigation 129, no. 1 (2019): 437. http://dx.doi.org/10.1172/jci126191.

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17

Guerra, Carmen, Paloma Navarro, Angela M. Valverde, et al. "Brown adipose tissue–specific insulin receptor knockout shows diabetic phenotype without insulin resistance." Journal of Clinical Investigation 108, no. 8 (2001): 1205–13. http://dx.doi.org/10.1172/jci13103.

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18

Elgadi, Aziz, Helen Zemack, Claude Marcus, and Svante Norgren. "Tissue-specific knockout of TSHr in white adipose tissue increases adipocyte size and decreases TSH-induced lipolysis." Biochemical and Biophysical Research Communications 393, no. 3 (2010): 526–30. http://dx.doi.org/10.1016/j.bbrc.2010.02.042.

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19

Cole, Justin M., Hong Xiao, Jonathan W. Adams, Kevin M. Disher, Hui Zhao, and Kenneth E. Bernstein. "New approaches to genetic manipulation of mice: tissue-specific expression of ACE." American Journal of Physiology-Renal Physiology 284, no. 4 (2003): F599—F607. http://dx.doi.org/10.1152/ajprenal.00308.2002.

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The renin-angiotensin system (RAS) plays a central role in body physiology, controlling blood pressure and blood electrolyte composition. ACE.1 (null) mice are null for all expression of angiotensin-converting enzyme (ACE). These mice have low blood pressure, the inability to concentrate urine, and a maldevelopment of the kidney. In contrast, ACE.2 (tissue null) mice produce one-third normal plasma ACE but no tissue ACE. They also have low blood pressure and cannot concentrate urine, but they have normal indices of renal function. These mice, while very informative, show that the null approach

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20

Murovets, V. O., E. A. Sozontov, and T. G. Zachepilo. "Effect of taste receptor protein T1R3 on the development of islet tissue of the murine pancreas." Доклады Академии наук 484, no. 1 (2019): 117–20. http://dx.doi.org/10.31857/s0869-56524841117-120.

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Protein T1R3, the main subunit of sweet, as well as amino acid, taste receptor, is expressed in the epithelium of the tongue and gastro intestinal tract, in β–cells of the pancreas, hypothalamus, and numerous other organs. Recently, convincing witnesses of T1R3 involvement in control of carbohydrate and lipid metabolism, and control of production of incretines and insulin, have been determined. In the study on Tas1r3-gene knockout mouse strain and parent strain C57Bl/6J as control, priority data concerning the effect of T1R3 on the morphological characteristics of Langerhans islets in the panc

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21

Skorobogatko, Yuliya, Morgan Dragan, Claudia Cordon, et al. "RalA controls glucose homeostasis by regulating glucose uptake in brown fat." Proceedings of the National Academy of Sciences 115, no. 30 (2018): 7819–24. http://dx.doi.org/10.1073/pnas.1801050115.

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Insulin increases glucose uptake into adipose tissue and muscle by increasing trafficking of the glucose transporter Glut4. In cultured adipocytes, the exocytosis of Glut4 relies on activation of the small G protein RalA by insulin, via inhibition of its GTPase activating complex RalGAP. Here, we evaluate the role of RalA in glucose uptake in vivo with specific chemical inhibitors and by generation of mice with adipocyte-specific knockout of RalGAPB. RalA was profoundly activated in brown adipose tissue after feeding, and its inhibition prevented Glut4 exocytosis. RalGAPB knockout mice with di

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22

Wu, Tong-Tong, Yuan-Wu Ma, Xu Zhang, et al. "Myocardial tissue-specific Dnmt1 knockout in rats protects against pathological injury induced by Adriamycin." Laboratory Investigation 100, no. 7 (2020): 974–85. http://dx.doi.org/10.1038/s41374-020-0402-y.

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23

Kos, Claudine H. "Methods in Nutrition Science: Cre/loxP System for Generating Tissue-specific Knockout Mouse Models." Nutrition Reviews 62, no. 6 (2004): 243–46. http://dx.doi.org/10.1111/j.1753-4887.2004.tb00046.x.

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24

Wolf, George. "Tissue-specific Knockout Defines Peroxisome Proliferator–activated Receptor Gamma Function in Muscle and Liver." Nutrition Reviews 62, no. 6 (2004): 253–55. http://dx.doi.org/10.1301/nr2004.jun253-255.

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25

Stephens, Jacqueline M., Jennifer L. Bailey, Hardy Hang, et al. "Adipose Tissue Dysfunction Occurs Independently of Obesity in Adipocyte‐Specific Oncostatin Receptor Knockout Mice." Obesity 26, no. 9 (2018): 1439–47. http://dx.doi.org/10.1002/oby.22254.

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26

Ishikawa, Tomo-o., and Harvey R. Herschman. "Conditional knockout mouse for tissue-specific disruption of the cyclooxygenase-2 (Cox-2) gene." genesis 44, no. 3 (2006): 143–49. http://dx.doi.org/10.1002/gene.20192.

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27

Scharfenberger, Lukas, Tina Hennerici, Gábor Király, Sophie Kitzmüller, Marigje Vernooij, and Julia G. Zielinski. "Transgenic Mouse Technology in Skin Biology: Generation of Complete or Tissue-Specific Knockout Mice." Journal of Investigative Dermatology 134, no. 1 (2014): 1–5. http://dx.doi.org/10.1038/jid.2013.457.

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28

Piprek, Rafal P., Michal Kolasa, Dagmara Podkowa, Malgorzata Kloc, and Jacek Z. Kubiak. "Tissue-specific knockout of E-cadherin (Cdh1) in developing mouse gonads causes germ cells loss." Reproduction 158, no. 2 (2019): 149–59. http://dx.doi.org/10.1530/rep-18-0621.

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The normal course of gonad development is critical for the sexual development and reproductive capacity of the individual. During development, an incipient bipotential gonad which consists of unorganized aggregate of cells, must differentiate into highly structured testis or ovary. Cell adhesion molecules (CAMs) are a group of proteins crucial for segregation and aggregation of different cell types to form different tissues. E-cadherin (Cdh1) is one of the CAMs expressed in the developing gonads. We used tissue-specific knockout of Cdh1 gene in OCT4+ germ cells and, separately, in SF1+ somatic

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29

Müller, Julia, Steffen Mayerl, Theo J. Visser, et al. "Tissue-Specific Alterations in Thyroid Hormone Homeostasis in Combined Mct10 and Mct8 Deficiency." Endocrinology 155, no. 1 (2014): 315–25. http://dx.doi.org/10.1210/en.2013-1800.

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The monocarboxylate transporter Mct10 (Slc16a10; T-type amino acid transporter) facilitates the cellular transport of thyroid hormone (TH) and shows an overlapping expression with the well-established TH transporter Mct8. Because Mct8 deficiency is associated with distinct tissue-specific alterations in TH transport and metabolism, we speculated that Mct10 inactivation may compromise the tissue-specific TH homeostasis as well. However, analysis of Mct10 knockout (ko) mice revealed normal serum TH levels and tissue TH content in contrast to Mct8 ko mice that are characterized by high serum T3,

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30

Wang, Wei, Xiao Hao, Lina Han, et al. "Tissue-Specific Ablation of ACSL4 Results in Disturbed Steroidogenesis." Endocrinology 160, no. 11 (2019): 2517–28. http://dx.doi.org/10.1210/en.2019-00464.

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Abstract ACSL4 is a member of the ACSL family that catalyzes the conversion of long-chain fatty acids to acyl-coenzyme As, which are essential for fatty-acid incorporation and utilization in diverse metabolic pathways, including cholesteryl ester synthesis. Steroidogenic tissues such as the adrenal gland are particularly enriched in cholesteryl esters of long-chain polyunsaturated fatty acids, which constitute an important pool supplying cholesterol for steroid synthesis. The current studies addressed whether ACSL4 is required for normal steroidogenesis. CYP11A1 promoter‒mediated Cre was used

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31

Yu, S., D. Yu, E. Lee, et al. "Variable and tissue-specific hormone resistance in heterotrimeric Gs protein -subunit (Gs ) knockout mice is due to tissue-specific imprinting of the Gs gene." Proceedings of the National Academy of Sciences 95, no. 15 (1998): 8715–20. http://dx.doi.org/10.1073/pnas.95.15.8715.

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32

Silva, José P., Martin Köhler, Caroline Graff та ін. "Impaired insulin secretion and β-cell loss in tissue-specific knockout mice with mitochondrial diabetes". Nature Genetics 26, № 3 (2000): 336–40. http://dx.doi.org/10.1038/81649.

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33

Lillis, Anna P., Lauren B. Van Duyn, Joanne E. Murphy-Ullrich, and Dudley K. Strickland. "LDL Receptor-Related Protein 1: Unique Tissue-Specific Functions Revealed by Selective Gene Knockout Studies." Physiological Reviews 88, no. 3 (2008): 887–918. http://dx.doi.org/10.1152/physrev.00033.2007.

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The LDL receptor-related protein (originally called LRP, but now referred to as LRP1) is a large endocytic receptor that is widely expressed in several tissues. LRP1 is a member of the LDL receptor family that plays diverse roles in various biological processes including lipoprotein metabolism, degradation of proteases, activation of lysosomal enzymes, and cellular entry of bacterial toxins and viruses. Deletion of the LRP1 gene leads to lethality in mice, revealing a critical, but as of yet, undefined role in development. Tissue-specific gene deletion studies reveal an important contribution

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34

Choi, Ran Hee, Abigail McConahay, Mackenzie B. Johnson, Ha-Won Jeong та Ho-Jin Koh. "Adipose tissue-specific knockout of AMPKα1/α2 results in normal AICAR tolerance and glucose metabolism". Biochemical and Biophysical Research Communications 519, № 3 (2019): 633–38. http://dx.doi.org/10.1016/j.bbrc.2019.09.049.

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35

Silva Barbosa, Anne C., Dong Zhou, Yang Xie, et al. "Inhibition of Estrogen Sulfotransferase (SULT1E1/EST) Ameliorates Ischemic Acute Kidney Injury in Mice." Journal of the American Society of Nephrology 31, no. 7 (2020): 1496–508. http://dx.doi.org/10.1681/asn.2019080767.

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BackgroundStudies have suggested that estrogens may protect mice from AKI. Estrogen sulfotransferase (SULT1E1, or EST) plays an important role in estrogen homeostasis by sulfonating and deactivating estrogens, but studies on the role of SULT1E1 in AKI are lacking.MethodsWe used the renal ischemia-reperfusion model to investigate the role of SULT1E1 in AKI. We subjected wild-type mice, Sult1e1 knockout mice, and Sult1e1 knockout mice with liver-specific reconstitution of SULT1E1 expression to bilateral renal ischemia-reperfusion or sham surgery, either in the absence or presence of gonadectomy.

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36

Everett, Lesley A., Audrey C. A. Cleuren, Rami N. Khoriaty, and David Ginsburg. "Murine coagulation factor VIII is synthesized in endothelial cells." Blood 123, no. 24 (2014): 3697–705. http://dx.doi.org/10.1182/blood-2014-02-554501.

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Key Points Lman1 tissue-specific knockout mice reveal that endothelial cells, not hepatocytes, are the primary source of FVIII biosynthesis. F8 gene expression is heterogeneous among endothelial cell populations in different tissues.

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37

Yu, I.-Chen, Hung-Yun Lin, Ning-Chun Liu, et al. "Hyperleptinemia without Obesity in Male Mice Lacking Androgen Receptor in Adipose Tissue." Endocrinology 149, no. 5 (2008): 2361–68. http://dx.doi.org/10.1210/en.2007-0516.

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Insulin resistance occurs through an inadequate response to insulin by insulin target organs such as liver, muscle, and adipose tissue with consequent insufficient glucose uptake. In previous studies we demonstrated that whole body androgen receptor (AR) knockout (AR−/y) mice develop obesity and exhibit insulin and leptin resistance at advanced age. By examining adipose tissue-specific AR knockout (A-AR−/y) mice, we found A-AR−/y mice were hyperleptinemic but showed no leptin resistance, although body weight and adiposity index of A-AR−/y mice were identical with those of male wild-type contro

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38

Orlanski, Shari, Verena Labi, Yitzhak Reizel, et al. "Tissue-specific DNA demethylation is required for proper B-cell differentiation and function." Proceedings of the National Academy of Sciences 113, no. 18 (2016): 5018–23. http://dx.doi.org/10.1073/pnas.1604365113.

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There is ample evidence that somatic cell differentiation during development is accompanied by extensive DNA demethylation of specific sites that vary between cell types. Although the mechanism of this process has not yet been elucidated, it is likely to involve the conversion of 5mC to 5hmC by Tet enzymes. We show that a Tet2/Tet3 conditional knockout at early stages of B-cell development largely prevents lineage-specific programmed demethylation events. This lack of demethylation affects the expression of nearby B-cell lineage genes by impairing enhancer activity, thus causing defects in B-c

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39

Haskins, Ryan M., Anh T. Nguyen, Gabriel F. Alencar, et al. "Klf4 has an unexpected protective role in perivascular cells within the microvasculature." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 2 (2018): H402—H414. http://dx.doi.org/10.1152/ajpheart.00084.2018.

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Recent smooth muscle cell (SMC) lineage-tracing studies have revealed that SMCs undergo remarkable changes in phenotype during development of atherosclerosis. Of major interest, we demonstrated that Kruppel-like factor 4 (KLF4) in SMCs is detrimental for overall lesion pathogenesis, in that SMC-specific conditional knockout of the KLF4 gene ( Klf4) resulted in smaller, more-stable lesions that exhibited marked reductions in the numbers of SMC-derived macrophage- and mesenchymal stem cell-like cells. However, since the clinical consequences of atherosclerosis typically occur well after our repr

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40

MOUCHEL, Nathalie, Sytse A. HENSTRA, Victoria A. McCARTHY, Sarah H. WILLIAMS, Marios PHYLACTIDES, and Ann HARRIS. "HNF1alpha is involved in tissue-specific regulation of CFTR gene expression." Biochemical Journal 378, no. 3 (2004): 909–18. http://dx.doi.org/10.1042/bj20031157.

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The CFTR (cystic fibrosis transmembrane conductance regulator) gene shows a complex pattern of expression with tissue-specific and temporal regulation. However, the genetic elements and transcription factors that control CFTR expression are largely unidentified. The CFTR promoter does not confer tissue specificity on gene expression, suggesting that there are regulatory elements outside the upstream region. Analysis of potential regulatory elements defined as DNase 1-hypersensitive sites within introns of the gene revealed multiple predicted binding sites for the HNF1α (hepatocyte nuclear fact

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41

Zhang, Zhao, Thomas Gallagher, Philipp E. Scherer, and Bruce Beutler. "Tissue-specific disruption ofKbtbd2uncovers adipocyte-intrinsic and -extrinsic features of theteenylipodystrophy syndrome." Proceedings of the National Academy of Sciences 117, no. 21 (2020): 11829–35. http://dx.doi.org/10.1073/pnas.2000118117.

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Loss of KBTBD2 in all tissues causes theteenyphenotype, characterized by insulin resistance with late failure of insulin production, severe hyperglycemia/diabetes, lipodystrophy, hepatosteatosis, and growth retardation. KBTBD2 maintains insulin sensitivity in adipocytes by restricting the abundance of p85α. However, the possible physiological contribution or contributions of KBTBD2 have not yet been examined in other tissues. Here we show that mice with an adipocyte-specific knockout ofKbtbd2accumulate p85α in white and brown adipose tissues, causing insulin resistance, moderate rather than se

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42

Watts, Jason S., Henry F. Harrison, Shizue Omi, et al. "New Strains for Tissue-Specific RNAi Studies in Caenorhabditis elegans." G3: Genes|Genomes|Genetics 10, no. 11 (2020): 4167–76. http://dx.doi.org/10.1534/g3.120.401749.

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RNA interference is a powerful tool for dissecting gene function. In Caenorhabditis elegans, ingestion of double stranded RNA causes strong, systemic knockdown of target genes. Further insight into gene function can be revealed by tissue-specific RNAi techniques. Currently available tissue-specific C. elegans strains rely on rescue of RNAi function in a desired tissue or cell in an otherwise RNAi deficient genetic background. We attempted to assess the contribution of specific tissues to polyunsaturated fatty acid (PUFA) synthesis using currently available tissue-specific RNAi strains. We disc

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43

DeLay, Bridget D., Mark E. Corkins, Hannah L. Hanania, et al. "Tissue-Specific Gene Inactivation in Xenopus laevis: Knockout of lhx1 in the Kidney with CRISPR/Cas9." Genetics 208, no. 2 (2017): 673–86. http://dx.doi.org/10.1534/genetics.117.300468.

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44

De Gendt, Karel, and Guido Verhoeven. "Tissue- and cell-specific functions of the androgen receptor revealed through conditional knockout models in mice." Molecular and Cellular Endocrinology 352, no. 1-2 (2012): 13–25. http://dx.doi.org/10.1016/j.mce.2011.08.008.

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45

Jain, Manu, Anna Lam та Cara J. Gottardi. "Tissue-Specific Knockout/Knockdown of Type 2 TGF-β Receptor and Protection against Bleomycin Injury/Fibrosis". American Journal of Respiratory and Critical Care Medicine 184, № 8 (2011): 983. http://dx.doi.org/10.1164/ajrccm.184.8.983.

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46

Sun, Xingshen, Hongshu Sui, Xiaoming Liu, et al. "Tissue-Specific Complementation of Intestinal Disease in a Transgenic CFTR-Knockout Ferret Model Generated by SCNT." Biology of Reproduction 83, Suppl_1 (2010): 401. http://dx.doi.org/10.1093/biolreprod/83.s1.401.

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47

CHOI, RAN HEE, ABIGAIL MCCONAHAY, MACKENZIE B. JOHNSON, and HO-JIN KOH. "Adipose Tissue–Specific Knockout of AMPK alpha1/alpha2 Results in Normal AICAR Tolerance and Glucose Metabolism." Diabetes 67, Supplement 1 (2018): 1753—P. http://dx.doi.org/10.2337/db18-1753-p.

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48

Zheng, Xiaohua, Edward B. Arias, Nathan R. Qi, Thomas L. Saunders, and Gregory D. Cartee. "In vivo glucoregulation and tissue-specific glucose uptake in female Akt substrate 160 kDa knockout rats." PLOS ONE 15, no. 2 (2020): e0223340. http://dx.doi.org/10.1371/journal.pone.0223340.

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49

Vanyai, Hannah K., Fabrice Prin, Oriane Guillermin, et al. "Control of skeletal morphogenesis by the Hippo-YAP/TAZ pathway." Development 147, no. 21 (2020): dev187187. http://dx.doi.org/10.1242/dev.187187.

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ABSTRACTThe Hippo-YAP/TAZ pathway is an important regulator of tissue growth, but can also control cell fate or tissue morphogenesis. Here, we investigate the function of the Hippo pathway during the development of cartilage, which forms the majority of the skeleton. Previously, YAP was proposed to inhibit skeletal size by repressing chondrocyte proliferation and differentiation. We find that, in vitro, Yap/Taz double knockout impairs murine chondrocyte proliferation, whereas constitutively nuclear nls-YAP5SA accelerates proliferation, in line with the canonical role of this pathway in most ti

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Feng, Chenchen, Chao Song, Yuejuan Liu, et al. "KnockTF: a comprehensive human gene expression profile database with knockdown/knockout of transcription factors." Nucleic Acids Research 48, no. D1 (2019): D93—D100. http://dx.doi.org/10.1093/nar/gkz881.

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Abstract Transcription factors (TFs) and their target genes have important functions in human diseases and biological processes. Gene expression profile analysis before and after knockdown or knockout is one of the most important strategies for obtaining target genes of TFs and exploring TF functions. Human gene expression profile datasets with TF knockdown and knockout are accumulating rapidly. Based on the urgent need to comprehensively and effectively collect and process these data, we developed KnockTF (http://www.licpathway.net/KnockTF/index.html), a comprehensive human gene expression pr

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