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Journal articles on the topic 'Knockin mouse model'

Author: Grafiati

Published: 18 May 2024

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1

Savva, Isavella, Charalampos Stefanou, Myrtani Pieri, et al. "MP036A NOVEL KNOCKIN MOUSE MODEL FOR ALPORT SYNDROME." Nephrology Dialysis Transplantation 31, suppl_1 (2016): i354. http://dx.doi.org/10.1093/ndt/gfw182.06.

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2

Luo, Yichen, Liang Du, Zhimeng Yao, et al. "Generation and Application of Inducible Chimeric RNA ASTN2-PAPPAas Knockin Mouse Model." Cells 11, no. 2 (2022): 277. http://dx.doi.org/10.3390/cells11020277.

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Chimeric RNAs (chiRNAs) play many previously unrecognized roles in different diseases including cancer. They can not only be used as biomarkers for diagnosis and prognosis of various diseases but also serve as potential therapeutic targets. In order to better understand the roles of chiRNAs in pathogenesis, we inserted human sequences into mouse genome and established a knockin mouse model of the tamoxifen-inducible expression of ASTN2-PAPPA antisense chimeric RNA (A-PaschiRNA). Mice carrying the A-PaschiRNA knockin gene do not display any apparent abnormalities in growth, fertility, histologi

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3

de Winter, J., M. Yuen, R. Van der Pijl, et al. "P.162Novel Kbtbd13R408C-knockin mouse model phenocopies NEM6 myopathy." Neuromuscular Disorders 29 (October 2019): S95. http://dx.doi.org/10.1016/j.nmd.2019.06.217.

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4

Wegener, Eike, Cornelia Brendel, Andre Fischer, Swen Hülsmann, Jutta Gärtner, and Peter Huppke. "Characterization of the MeCP2R168X Knockin Mouse Model for Rett Syndrome." PLoS ONE 9, no. 12 (2014): e115444. http://dx.doi.org/10.1371/journal.pone.0115444.

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5

Rose, Samuel J., Lisa H. Kriener, Ann K. Heinzer, et al. "The first knockin mouse model of episodic ataxia type 2." Experimental Neurology 261 (November 2014): 553–62. http://dx.doi.org/10.1016/j.expneurol.2014.08.001.

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6

Sundberg, J. P., C. H. Pratt, K. A. Silva, et al. "394 Card14 knockin mouse model of psoriasis and psoriatic arthritis." Journal of Investigative Dermatology 136, no. 5 (2016): S70. http://dx.doi.org/10.1016/j.jid.2016.02.428.

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7

Baelde, R., A. Fortes Monteiro, E. Nollet, et al. "P400 Kbtbd13R408C-knockin mouse model elucidates mitochondrial pathomechanism in NEM6." Neuromuscular Disorders 33 (October 2023): S123. http://dx.doi.org/10.1016/j.nmd.2023.07.231.

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8

Yuan, Weiming, Xiangshu Wen, Ping Rao, Seil Kim, and Peter Cresswell. "Characterization of a human CD1d-knockin mouse (106.44)." Journal of Immunology 188, no. 1_Supplement (2012): 106.44. http://dx.doi.org/10.4049/jimmunol.188.supp.106.44.

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Abstract CD1d-restricted natural killer T (NKT) cells regulate the immune system in response to a broad range of diseases. The CD1d/NKT antigen presentation pathway is largely conserved between human and mouse, however, there is distinct difference between the two species. To better study human CD1d antigen presentation in an in vivo setting, we have generated a human CD1d knock-in (KI) mouse. We have expressed human CD1d (hCD1d) in place of mouse CD1d (mCD1d). The expression of hCD1d was verified on CD4+CD8+DP thymocytes and thymic dendritic cells, which are involved in NKT cell positive and

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9

Guo, Qinxi, Hui Zheng, and Nicholas John Justice. "Central CRF system perturbation in an Alzheimer's disease knockin mouse model." Neurobiology of Aging 33, no. 11 (2012): 2678–91. http://dx.doi.org/10.1016/j.neurobiolaging.2012.01.002.

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10

Nomura, Naohiro, Masato Tajima, Noriko Sugawara, et al. "Generation and analyses of R8L barttin knockin mouse." American Journal of Physiology-Renal Physiology 301, no. 2 (2011): F297—F307. http://dx.doi.org/10.1152/ajprenal.00604.2010.

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Barttin, a gene product of BSND, is one of four genes responsible for Bartter syndrome. Coexpression of barttin with ClC-K chloride channels dramatically induces the expression of ClC-K current via insertion of ClC-K-barttin complexes into plasma membranes. We previously showed that stably expressed R8L barttin, a disease-causing missense mutant, is retained in the endoplasmic reticulum (ER) of Madin-Darby canine kidney (MDCK) cells, with the barttin β-subunit remaining bound to ClC-K α-subunits (Hayama A, Rai T, Sasaki S, Uchida S. Histochem Cell Biol 119: 485–493, 2003). However, transient e

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11

Hammersen, Johanna, Jin Hou, Stephanie Wünsche, Sven Brenner, Thomas Winkler, and Holm Schneider. "A new mouse model of junctional epidermolysis bullosa: the LAMB3 628G>A knockin mouse." Molecular and Cellular Pediatrics 1, Suppl 1 (2014): A12. http://dx.doi.org/10.1186/2194-7791-1-s1-a12.

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12

Hammersen, Johanna, Jin Hou, Stephanie Wünsche, Sven Brenner, Thomas Winkler, and Holm Schneider. "A New Mouse Model of Junctional Epidermolysis Bullosa: The LAMB3 628G>A Knockin Mouse." Journal of Investigative Dermatology 135, no. 3 (2015): 921–24. http://dx.doi.org/10.1038/jid.2014.466.

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13

Yan, Dongqing, Robert E. Hutchison, and Golam Mohi. "Critical requirement for Stat5 in a mouse model of polycythemia vera." Blood 119, no. 15 (2012): 3539–49. http://dx.doi.org/10.1182/blood-2011-03-345215.

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The JAK2V617F mutation has been identified in most cases of Ph-negative myeloproliferative neoplasms (MPNs) including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). Expression of JAK2V617F results in constitutive activation of multiple signaling molecules/pathways. However, the key signaling downstream of JAK2V617F required for transformation and induction of MPNs remains elusive. Using a mouse genetic strategy, we show here that Stat5 is absolutely required for the pathogenesis of PV induced by Jak2V617F. Whereas expression of Jak2V617F in mice result

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14

Ellegood, Jacob, Jason P. Lerch, and R. Mark Henkelman. "Brain abnormalities in a Neuroligin3 R451C knockin mouse model associated with autism." Autism Research 4, no. 5 (2011): 368–76. http://dx.doi.org/10.1002/aur.215.

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15

Gilley, Jonathan, Robert Adalbert, and Michael P. Coleman. "Modelling early responses to neurodegenerative mutations in mice." Biochemical Society Transactions 39, no. 4 (2011): 933–38. http://dx.doi.org/10.1042/bst0390933.

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Considering the many differences between mice and humans, it is perhaps surprising how well mice model late-onset human neurodegenerative disease. Models of Alzheimer's disease, frontotemporal dementia, Parkinson's disease and Huntington's disease show some striking similarities to the corresponding human pathologies in terms of axonal transport disruption, protein aggregation, synapse loss and some behavioural phenotypes. However, there are also major differences. To extrapolate from mouse models to human disease, we need to understand how these differences relate to intrinsic limitations of

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16

Ohno, Shinji, Nobuyuki Ono, Fumio Seki, et al. "Measles Virus Infection of SLAM (CD150) Knockin Mice Reproduces Tropism and Immunosuppression in Human Infection." Journal of Virology 81, no. 4 (2006): 1650–59. http://dx.doi.org/10.1128/jvi.02134-06.

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ABSTRACT The human signaling lymphocyte activation molecule (SLAM, also called CD150), a regulator of antigen-driven T-cell responses and macrophage functions, acts as a cellular receptor for measles virus (MV), and its V domain is necessary and sufficient for receptor function. We report here the generation of SLAM knockin mice in which the V domain of mouse SLAM was replaced by that of human SLAM. The chimeric SLAM had an expected distribution and normal function in the knockin mice. Splenocytes from the SLAM knockin mice permitted the in vitro growth of a virulent MV strain but not that of

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17

van den Maagdenberg, Arn M. J. M., Daniela Pietrobon, Tommaso Pizzorusso, et al. "A Cacna1a Knockin Migraine Mouse Model with Increased Susceptibility to Cortical Spreading Depression." Neuron 41, no. 5 (2004): 701–10. http://dx.doi.org/10.1016/s0896-6273(04)00085-6.

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18

Qin, Mei, Tianjian Huang, Zhonghua Liu, et al. "Cerebral Protein Synthesis in a Knockin Mouse Model of the Fragile X Premutation." ASN Neuro 6, no. 5 (2014): 175909141455195. http://dx.doi.org/10.1177/1759091414551957.

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19

Wu, Fenfen, Wentao Mi, Dennis K. Burns, et al. "A sodium channel knockin mutant (NaV1.4-R669H) mouse model of hypokalemic periodic paralysis." Journal of Clinical Investigation 121, no. 10 (2011): 4082–94. http://dx.doi.org/10.1172/jci57398.

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20

Turnes, Bruna, Leo Mejia, Carl Nist-Lund, et al. "NEWLY DEVELOPED TECPR2 KNOCKIN MOUSE MODEL FOR THE STUDY OF TECPR2-RELATED DISORDER." IBRO Neuroscience Reports 15 (October 2023): S145. http://dx.doi.org/10.1016/j.ibneur.2023.08.189.

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21

Nirala, Bikesh Kumar, Lyazat Kurenbekova, Tajhal Patel, et al. "Abstract 6713: Myc-regulated miR17, 20a modulate RANK expression in osteosarcoma." Cancer Research 83, no. 7_Supplement (2023): 6713. http://dx.doi.org/10.1158/1538-7445.am2023-6713.

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Abstract Osteosarcoma (OS) is the most common primary bone tumor in children and adolescents. Approximately 25-30% of these tumors carry amplification of chromosome 8q24, which harbors the oncogene c-Myc, and correlates with a poor prognosis in patients with OS. To understand the mechanisms that underlie the ability of Myc to alter both the tumor and its surrounding tumor immune microenvironment (TiME), we generated and molecularly characterized an osteoblast-specific Cre-Lox-Stop-Lox;(LSL)-c-MycT58A;p53f/+ knockin genetically engineered mouse model (GEMM). Phenotypically, the Myc knockin-GEMM

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22

Liu, Yuning, Hong Xing, Bradley J. Wilkes, et al. "The abnormal firing of Purkinje cells in the knockin mouse model of DYT1 dystonia." Brain Research Bulletin 165 (December 2020): 14–22. http://dx.doi.org/10.1016/j.brainresbull.2020.09.011.

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23

Fan, Changfa, Xi Wu, Qiang Liu, et al. "A Human DPP4-Knockin Mouse’s Susceptibility to Infection by Authentic and Pseudotyped MERS-CoV." Viruses 10, no. 9 (2018): 448. http://dx.doi.org/10.3390/v10090448.

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Infection by the Middle East respiratory syndrome coronavirus (MERS-CoV) causes respiratory illness and has a high mortality rate (~35%). The requirement for the virus to be manipulated in a biosafety level three (BSL-3) facility has impeded development of urgently-needed antiviral agents. Here, we established anovel mouse model by inserting human dipeptidyl peptidase 4 (hDPP4) into the Rosa26 locus using CRISPR/Cas9, resulting in global expression of the transgene in a genetically stable mouse line. The mice were highly susceptible to infection by MERS-CoV clinical strain hCoV-EMC, which indu

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24

He, Daniel. "Abstract 5092: Non-IL-2 blocking Treg-depleting anti-human CD25 mAb primes potent anti-tumor immunity and synergizes anti-tumor effects of anti-PD-1 in a novel hIL-2RA knockin model." Cancer Research 83, no. 7_Supplement (2023): 5092. http://dx.doi.org/10.1158/1538-7445.am2023-5092.

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Abstract The therapeutic effects for cancer immunotherapy are largely hampered by intratumoral CD4+CD25+ regulatory T cells (Tregs) which leads to poor outcome in many cancer patients upon treatment of immune checkpoint inhibitors. Moreover, the balance between effector T (Teff) cells and Treg cells in the tumor microenvironment (TME) impacts on tumor progression and anti-tumor immunity. Depleting tumor-infiltrating Tregs by selectively targeting CD25 to reduce the ratios of regulatory to effector T cells (Treg/Teff) without disturbing IL-2 signalling is a promising strategy to advance anti-tu

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25

Rongvaux, Anthony, Tim Willinger, Hitoshi Takizawa, et al. "Human thrombopoietin knockin mice efficiently support human hematopoiesis in vivo (153.5)." Journal of Immunology 186, no. 1_Supplement (2011): 153.5. http://dx.doi.org/10.4049/jimmunol.186.supp.153.5.

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Abstract Hematopoietic stem cells (HSCs) both self-renew and give rise to all blood cells for the lifetime of an individual. Xenogeneic mouse models are broadly used to study human hematopoietic stem and progenitor cell biology in vivo. However, maintenance, differentiation, and function of human hematopoietic cells is suboptimal in these hosts. We hypothesized that this defect was due to reduced cross-reactivity of mouse cytokines on the human receptor. Thrombopoietin (TPO) has been demonstrated as a crucial cytokine supporting maintenance and self-renewal of HSCs. We generated RAG2-/-γc-/- m

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26

Seo, Kyowon, Eun Kyoung Kim, Jaeil Choi, Dae-Seong Kim, and Jin-Hong Shin. "Functional recovery of a novel knockin mouse model of dysferlinopathy by readthrough of nonsense mutation." Molecular Therapy - Methods & Clinical Development 21 (June 2021): 702–9. http://dx.doi.org/10.1016/j.omtm.2021.04.015.

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27

Bonnet, Marie, Fang Huang, Touati Benoukraf та ін. "Duality of Enhancer Functioning Mode Revealed in a Reduced TCRβ Gene Enhancer Knockin Mouse Model". Journal of Immunology 183, № 12 (2009): 7939–48. http://dx.doi.org/10.4049/jimmunol.0902179.

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28

Mohamed, Rasha M. S. M., Sachio Morimoto, Islam A. A. E. H. Ibrahim та ін. "GSK-3β heterozygous knockout is cardioprotective in a knockin mouse model of familial dilated cardiomyopathy". American Journal of Physiology-Heart and Circulatory Physiology 310, № 11 (2016): H1808—H1815. http://dx.doi.org/10.1152/ajpheart.00771.2015.

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Glycogen synthase kinase-3β (GSK-3β) plays a central role in both cardiac physiology and pathology. Herein we want to clarify the role of GSK-3β in familial dilated cardiomyopathy. We generated a mouse model carrying a heterozygous knockout mutation of GSK-3β (GSK-3β+/− KO), together with a ΔK210 knockin mutation in cardiac troponin T (ΔK210 cTnT KI), which was proved to be one of the genetic causes of familial dilated cardiomyopathy (DCM). GSK-3β+/− KO prevented the slow and rapid deterioration in left ventricular systolic function accompanying heart failure (HF) in DCM mice with heterozygous

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29

Yang, Sung-Sen, Tetsuji Morimoto, Tatemitsu Rai, et al. "Molecular Pathogenesis of Pseudohypoaldosteronism Type II: Generation and Analysis of a Wnk4D561A/+ Knockin Mouse Model." Cell Metabolism 5, no. 5 (2007): 331–44. http://dx.doi.org/10.1016/j.cmet.2007.03.009.

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30

Baelde, R., V. Janssen, A. Fortes Monteiro, et al. "P407 Kbtbd13R408C-knockin mouse model reveals impaired relaxation kinetics as novel pathomechanism for NEM6 cardiomyopathy." Neuromuscular Disorders 33 (October 2023): S125. http://dx.doi.org/10.1016/j.nmd.2023.07.238.

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31

Valenzuela, Alicia, Karen Fancher, Cat Lutz, and Stephen Rockwood. "Mouse Models for Immunology Research available from The Jackson Laboratory Repository." Journal of Immunology 198, no. 1_Supplement (2017): 121.17. http://dx.doi.org/10.4049/jimmunol.198.supp.121.17.

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Abstract The Jackson Laboratory Repository serves as a centralized facility for the development, distribution and cryopreservation of mouse models of human biology and disease. Hundreds of new strains are added annually to one of the largest collections of characterized mouse strains available. Our newest strains carry genes associated with T lymphocyte regulation and development. T cells from the Fyb (ADAP) knockout (KO) exhibit impaired proliferation and TCR-mediated adhesion. T cells from the Cd27 KO have a diminished viral response and a delayed memory cell response. A conditional KO of Kd

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32

Zhao, Ling, Lemlem Alemu, Jun Cheng, Tao Zhen, Alan D. Friedman та Pu Paul Liu. "Functional Dissection of the C Terminus of CBFβ-SMMHC Indicates a Critical Role of the Multimerization Domain during Hematopoiesis and Leukemogenesis". Blood 124, № 21 (2014): 2218. http://dx.doi.org/10.1182/blood.v124.21.2218.2218.

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Abstract The recurrent chromosome 16 inversion (inv(16)) in acute myeloid leukemia (AML) subtype M4Eo results in a fusion between CBFB and MYH11 genes, which encodes a chimeric protein CBFβ-SMMHC (core binding factor β - smooth muscle myosin heavy chain). We previously generated mouse CBFB-MYH11 knock-in models that mimic the human inv(16) AML and demonstrated that the CBFβ-SMMHC fusion protein blocks RUNX1 and CBFβ function during definitive hematopoiesis and plays a driving role in leukemogenesis. Our recent studies indicated that the C-terminus of CBFβ-SMMHC, which contains domains for mult

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33

Shimura, Daisuke, Yoichiro Kusakari, Tetsuo Sasano, et al. "Heterozygous deletion of sarcolipin maintains normal cardiac function." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 1 (2016): H92—H103. http://dx.doi.org/10.1152/ajpheart.00411.2015.

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Sarcolipin (SLN) is a small proteolipid and a regulator of sarco(endo)plasmic reticulum Ca2+-ATPase. In heart tissue, SLN is exclusively expressed in the atrium. Previously, we inserted Cre recombinase into the endogenous SLN locus by homologous recombination and succeeded in generating SLN-Cre knockin (SlnCre/+) mice. This SlnCre/+ mouse can be used to generate an atrium-specific gene-targeting mutant, and it is based on the Cre-loxP system. In the present study, we used adult SlnCre/+ mice atria and analyzed the effects of heterozygous SLN deletion by Cre knockin before use as the gene targe

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34

Price, Brandee A., Ivette M. Sandoval, Fung Chan, et al. "Mislocalization and Degradation of Human P23H-Rhodopsin-GFP in a Knockin Mouse Model of Retinitis Pigmentosa." Investigative Opthalmology & Visual Science 52, no. 13 (2011): 9728. http://dx.doi.org/10.1167/iovs.11-8654.

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35

Ludwig, Michael R., Kyoko Kojima, Gregory J. Bowersock, et al. "Surveying the serologic proteome in a tissue-specific kras(G12D) knockin mouse model of pancreatic cancer." PROTEOMICS 16, no. 3 (2016): 516–31. http://dx.doi.org/10.1002/pmic.201500133.

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36

Li, Kun, Christine L. Wohlford-Lenane, Rudragouda Channappanavar, et al. "Mouse-adapted MERS coronavirus causes lethal lung disease in human DPP4 knockin mice." Proceedings of the National Academy of Sciences 114, no. 15 (2017): E3119—E3128. http://dx.doi.org/10.1073/pnas.1619109114.

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The Middle East respiratory syndrome (MERS) emerged in Saudi Arabia in 2012, caused by a zoonotically transmitted coronavirus (CoV). Over 1,900 cases have been reported to date, with ∼36% fatality rate. Lack of autopsies from MERS cases has hindered understanding of MERS-CoV pathogenesis. A small animal model that develops progressive pulmonary manifestations when infected with MERS-CoV would advance the field. As mice are restricted to infection at the level of DPP4, the MERS-CoV receptor, we generated mice with humanized exons 10–12 of the mouse Dpp4 locus. Upon inoculation with MERS-CoV, hu

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37

Santillo, Alessandra, Sara Falvo, Massimo Venditti, et al. "D-Aspartate Depletion Perturbs Steroidogenesis and Spermatogenesis in Mice." Biomolecules 13, no. 4 (2023): 621. http://dx.doi.org/10.3390/biom13040621.

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High levels of free D-aspartate (D-Asp) are present in vertebrate testis during post-natal development, coinciding with the onset of testosterone production, which suggests that this atypical amino acid might participate in the regulation of hormone biosynthesis. To elucidate the unknown role of D-Asp on testicular function, we investigated steroidogenesis and spermatogenesis in a one-month-old knockin mouse model with the constitutive depletion of D-Asp levels due to the targeted overexpression of D-aspartate oxidase (DDO), which catalyzes the deaminative oxidation of D-Asp to generate the co

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38

Rongvaux, Anthony, Tim Willinger, Hitoshi Takizawa, et al. "Human Thrombopoietin Knockin Mice Efficiently Support Human Hematopoiesis In Vivo." Blood 116, no. 21 (2010): 403. http://dx.doi.org/10.1182/blood.v116.21.403.403.

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Abstract Abstract 403 Hematopoietic stem cells (HSCs) both self-renew and give rise to all blood cells for the lifetime of an individual. Xenogeneic mouse models are currently broadly used to experimentally study human hematopoietic stem and progenitor cell biology in vivo. However, maintenance, differentiation, and function of human hematopoietic cells are suboptimal in these hosts. More specifically, (i) human cell engraftment is only transient, not lasting for the life of recipient mice, (ii) there is an unphysiological bias towards the lymphoid lineage as well as poor differentiation of my

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39

Duan, Wenming, Manal Y. Gabril, Madeleine Moussa, et al. "Knockin of SV40 Tag oncogene in a mouse adenocarcinoma of the prostate model demonstrates advantageous features over the transgenic model." Oncogene 24, no. 9 (2005): 1510–24. http://dx.doi.org/10.1038/sj.onc.1208229.

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40

van Oort, Ralph J., Jonathan L. Respress, Na Li, et al. "Accelerated Development of Pressure Overload–Induced Cardiac Hypertrophy and Dysfunction in an RyR2-R176Q Knockin Mouse Model." Hypertension 55, no. 4 (2010): 932–38. http://dx.doi.org/10.1161/hypertensionaha.109.146449.

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41

Zhao, Baobing, Yang Mei, Ronen Sumagin, et al. "Pleckstrin-2 Plays an Essential Role in the Pathogenesis of JAK2V617F-Induced Myeloproliferative Neoplasms." Blood 128, no. 22 (2016): 798. http://dx.doi.org/10.1182/blood.v128.22.798.798.

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Abstract V617F driver mutation of JAK2 is the leading cause of the Philadelphia-chromosome-negative myeloproliferative neoplasms (MPNs). Studies on the pathogenesis of JAK2V617F positive MPNs have primarily focused on deregulation of JAK2 and STAT activities. It remains unclear exactly how JAK2-STAT downstream targets are involved in the development of the MPNs. We previously reported that pleckstrin-2 (Plek2) plays an important role in terminal erythropoiesis in vitro. Here we show that Plek2 is a downstream target of the JAK2-STAT5 pathway in erythroid, megakaryocytic, and granulocytic cells

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42

Kim, Caroline S., Vasily V. Vasko, Yasuhito Kato, et al. "AKT Activation Promotes Metastasis in a Mouse Model of Follicular Thyroid Carcinoma." Endocrinology 146, no. 10 (2005): 4456–63. http://dx.doi.org/10.1210/en.2005-0172.

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The phosphatidylinositol 3-kinase/AKT pathway is crucial to many cell functions, and its dysregulation in tumors is a common finding. The molecular basis of follicular thyroid cancer metastasis is not well understood but may also be influenced by AKT activation. We previously created a knockin mutant mouse that expresses a mutant thyroid hormone receptor-β gene (TRβPV mouse) that spontaneously develops thyroid cancer and distant metastasis similar to human follicular thyroid cancer. In this study, we investigated whether our mouse model exhibits similar AKT activation as human follicular thyro

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43

mora, conchi, Ainhoa Garcia, Nuria Marzo, et al. "Role of Cdk4 in immunological tolerance and in pancreatic beta cell mass homeostasis in T1D (99.14)." Journal of Immunology 182, no. 1_Supplement (2009): 99.14. http://dx.doi.org/10.4049/jimmunol.182.supp.99.14.

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Abstract Cdk4 plays a central role in perinatal pancreatic β cell replication and is also highly expressed in healthy, adult human pancreatic beta cells. We have previously reported that, when the hyperactive mutant form of Cdk4, Cdk4R24C replaces the wild type gene, it causes β cell hyperplasia without promoting hypoglycemia in a non-autoimmune-prone mouse strain. We found out that when the mutant Cdk4R24C knockin model is backcrossed onto the NOD genetic background, diabetes is exacerbated due to the expression of the mutated Cdk4R24C form in the NOD immune system too, as in the absence of N

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44

Zhao, Xiaofeng, Xu Peng, Shaogang Sun, Ann Y. J. Park, and Jun-Lin Guan. "Role of kinase-independent and -dependent functions of FAK in endothelial cell survival and barrier function during embryonic development." Journal of Cell Biology 189, no. 6 (2010): 955–65. http://dx.doi.org/10.1083/jcb.200912094.

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Focal adhesion kinase (FAK) is essential for vascular development as endothelial cell (EC)–specific knockout of FAK (conditional FAK knockout [CFKO] mice) leads to embryonic lethality. In this study, we report the differential kinase-independent and -dependent functions of FAK in vascular development by creating and analyzing an EC-specific FAK kinase-defective (KD) mutant knockin (conditional FAK knockin [CFKI]) mouse model. CFKI embryos showed apparently normal development through embryonic day (E) 13.5, whereas the majority of CFKO embryos died at the same stage. Expression of KD FAK revers

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45

Datta, Nabanita S., Tareq A. Samra, and Abdul B. Abou-Samra. "Parathyroid hormone induces bone formation in phosphorylation-deficient PTHR1 knockin mice." American Journal of Physiology-Endocrinology and Metabolism 302, no. 10 (2012): E1183—E1188. http://dx.doi.org/10.1152/ajpendo.00380.2011.

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Activation of G protein-coupled receptors by agonists leads to receptor phosphorylation, internalization of ligand receptor complexes, and desensitization of hormonal response. The role of parathyroid hormone (PTH) receptor 1, PTHR1, is well characterized and known to regulate cellular responsiveness in vitro. However, the role of PTHR1 phosphorylation in bone formation is yet to be investigated. We have previously demonstrated that impaired internalization and sustained cAMP stimulation of phosphorylation-deficient (PD) PTHR1 leads to exaggerated cAMP response to subcutaneous PTH infusion in

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Volta, Mattia, and Heather Melrose. "LRRK2 mouse models: dissecting the behavior, striatal neurochemistry and neurophysiology of PD pathogenesis." Biochemical Society Transactions 45, no. 1 (2017): 113–22. http://dx.doi.org/10.1042/bst20160238.

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Abstract:

Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common genetic cause of familial Parkinson's disease (PD), resembling the sporadic disorder. Intensive effort has been directed toward LRRK2 mouse modeling and investigation, aimed at reproducing the human disease to inform mechanistic studies of pathogenesis and design of neuroprotective therapies. The physiological function of LRRK2 is still under exploration, but a clear role in striatal neurophysiology and animal behavior has emerged. Alterations in LRRK2 impair dopamine (DA) transmission, regulation and signaling, in addition

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Unno, T., M. Wakamori, M. Koike, et al. "Development of Purkinje cell degeneration in a knockin mouse model reveals lysosomal involvement in the pathogenesis of SCA6." Proceedings of the National Academy of Sciences 109, no. 43 (2012): 17693–98. http://dx.doi.org/10.1073/pnas.1212786109.

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Zhao, L., H. Alkadi, E. M. Kwon та ін. "The C-terminal multimerization domain is essential for leukemia development by CBFβ-SMMHC in a mouse knockin model". Leukemia 31, № 12 (2017): 2841–44. http://dx.doi.org/10.1038/leu.2017.262.

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Deng, Yun-Ping, and Anton Reiner. "Cholinergic interneurons in the Q140 knockin mouse model of Huntington's disease: Reductions in dendritic branching and thalamostriatal input." Journal of Comparative Neurology 524, no. 17 (2016): 3518–29. http://dx.doi.org/10.1002/cne.24013.

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Charbonneau, Noe L., Elise C. Manalo, Sara F. Tufa, et al. "Fibrillin‐1 in the Vasculature: In Vivo Accumulation of eGFP‐Tagged Fibrillin‐1 in a Knockin Mouse Model." Anatomical Record 303, no. 6 (2019): 1590–603. http://dx.doi.org/10.1002/ar.24217.

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