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https://www.readbyqxmd.com/read/27912078/mouse-double-minute-2-homolog-actively-suppresses-p53-activity-in-oocytes-during-mouse-folliculogenesis
#1
Chen-Xi Zhang, Qin Zhang, Yin-Yin Xie, Xue-Yan He, Cong Xiang, Xiao-Shuang Hou, Ying Zhou, Lai Chen, Guo-Xin Zhang, Geng Liu
The p53 signaling network is indispensible in cellular stress responses and tumor suppression. Negative regulations of p53 by mouse double minute 2 and 4 homologs (MDM2) and (MDM4) are an integrated component of the network and have been implicated in regulating the stress responses and the maintenance of normal development and homeostasis of multiple somatic cell lineages. However, the regulatory role of MDM2 on p53 and stress responses in female germ cells remains undetermined. Here, we used the Cre-loxP system to delete Mdm2 in oocytes at different stages of folliculogenesis in mice...
November 29, 2016: American Journal of Pathology
https://www.readbyqxmd.com/read/27911782/egfr-signaling-is-critical-for-maintaining-the-superficial-layer-of-articular-cartilage-and-preventing-osteoarthritis-initiation
#2
Haoruo Jia, Xiaoyuan Ma, Wei Tong, Basak Doyran, Zeyang Sun, Luqiang Wang, Xianrong Zhang, Yilu Zhou, Farid Badar, Abhishek Chandra, X Lucas Lu, Yang Xia, Lin Han, Motomi Enomoto-Iwamoto, Ling Qin
Osteoarthritis (OA) is the most common joint disease, characterized by progressive destruction of the articular cartilage. The surface of joint cartilage is the first defensive and affected site of OA, but our knowledge of genesis and homeostasis of this superficial zone is scarce. EGFR signaling is important for tissue homeostasis. Immunostaining revealed that its activity is mostly dominant in the superficial layer of healthy cartilage but greatly diminished when OA initiates. To evaluate the role of EGFR signaling in the articular cartilage, we studied a cartilage-specific Egfr-deficient (CKO) mouse model (Col2-Cre EgfrWa5/flox)...
November 28, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27909303/conditional-knockout-of-n-wasp-in-mouse-fibroblast-caused-keratinocyte-hyper-proliferation-and-enhanced-wound-closure
#3
Neeraj Jain, Pazhanichamy Kalailingam, Kai Wei Tan, Hui Bing Tan, Ming Keat Sng, Jeremy Soon Kiat Chan, Nguan Soon Tan, Thirumaran Thanabalu
Neural-Wiskott Aldrich Syndrome Protein (N-WASP) is expressed ubiquitously, regulates actin polymerization and is essential during mouse development. We have previously shown that N-WASP is critical for cell-ECM adhesion in fibroblasts. To characterize the role of N-WASP in fibroblast for skin development, we generated a conditional knockout mouse model in which fibroblast N-WASP was ablated using the Cre recombinase driven by Fibroblast Specific Protein promoter (Fsp-Cre). N-WASP(FKO) (N-WASP(fl/fl); Fsp-cre) were born following Mendelian genetics, survived without any visible abnormalities for more than 1 year and were sexually reproductive, suggesting that expression of N-WASP in fibroblast is not critical for survival under laboratory conditions...
December 2, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27907249/grainyhead-like-3-grhl3-deficiency-in-brain-leads-to-altered-locomotor-activity-and-decreased-anxiety-like-behaviours-in-aged-mice
#4
Sebastian Dworkin, Alana Auden, Darren D Partridge, Maria Daglas, Robert L Medcalf, Theo Mantamadiotis, Smitha R Georgy, Charbel Darido, Stephen M Jane, Stephen B Ting
The highly conserved Grainyhead-like (Grhl) family of transcription factors, comprising three members in vertebrates (Grhl1-3), play critical regulatory roles during embryonic development, cellular proliferation and apoptosis. Although loss of Grhl function leads to multiple neural abnormalities in numerous animal models, a comprehensive analysis of Grhl expression and function in the mammalian brain has not been reported. Here we show that only Grhl3 expression is detectable in the embryonic mouse brain; particularly within the habenula, an organ known to modulate repressive behaviours...
December 1, 2016: Developmental Neurobiology
https://www.readbyqxmd.com/read/27906081/vacht-overexpression-increases-acetylcholine-at-the-synaptic-cleft-and-accelerates-aging-of-neuromuscular-junctions
#5
Satoshi Sugita, Leland L Fleming, Caleb Wood, Sydney K Vaughan, Matheus P S M Gomes, Wallace Camargo, Ligia A Naves, Vania F Prado, Marco A M Prado, Cristina Guatimosim, Gregorio Valdez
BACKGROUND: Cholinergic dysfunction occurs during aging and in a variety of diseases, including amyotrophic lateral sclerosis (ALS). However, it remains unknown whether changes in cholinergic transmission contributes to age- and disease-related degeneration of the motor system. Here we investigated the effect of moderately increasing levels of synaptic acetylcholine (ACh) on the neuromuscular junction (NMJ), muscle fibers, and motor neurons during development and aging and in a mouse model for amyotrophic lateral sclerosis (ALS)...
October 5, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27896618/loss-of-liver-kinase-b1-causes-planar-polarity-defects-in-cochlear-hair-cells-in-mice
#6
Yuqin Men, Aizhen Zhang, Liwen Zhang, Yecheng Jin, Zhishuo Wang, Jing Zhao, Xiaolin Yu, Jian Zhang, Jiangang Gao
The tumor suppressor gene liver kinase B1 (LKB1), also called STK11, encodes a serine/threonine kinase. LKB1 plays crucial roles in cell differentiation, proliferation, and polarity. In this study, LKB1 conditional knockout mice (LKB1(Pax2) CKO mice) were generated using Pax2-Cre mice to investigate the function of LKB1 in inner ear hair cells during early embryonic period. LKB1(Pax2) CKO mice died perinatally. Immunofluorescence and scanning electron microscopy revealed that stereociliary bundles in LKB1(Pax2) CKO mice were clustered and misoriented, respectively...
November 28, 2016: Frontiers of Medicine
https://www.readbyqxmd.com/read/27881487/osteogenesis-requires-fak-dependent-collagen-synthesis-by-fibroblasts-and-osteoblasts
#7
Dhaarmini Rajshankar, Yongqiang Wang, Christopher A McCulloch
Focal adhesion kinase (FAK) is critical in adhesion-dependent signaling, but its role in osteogenesis in vivo is ill defined. We deleted Fak in fibroblasts and osteoblasts in Floxed-Fak mice bred with those expressing Cre-recombinase driven by 3.6 kb α1(I)-collagen promoter. Compared with wild-type (WT), conditional FAK-knockout (CFKO) mice were shorter (2-fold; P < 0.0001) and had crooked, shorter tails (50%; P < 0.0001). Microcomputed tomography analysis showed reduced bone volume (4-fold in tails; P < 0...
November 23, 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/27876863/intestinal-tuft-cells-regulate-the-atm-mediated-dna-damage-response-via-dclk1-dependent-mechanism-for-crypt-restitution-following-radiation-injury
#8
Parthasarathy Chandrakesan, Randal May, Nathaniel Weygant, Dongfeng Qu, William L Berry, Sripathi M Sureban, Naushad Ali, Chinthalapally Rao, Mark Huycke, Michael S Bronze, Courtney W Houchen
Crypt epithelial survival and regeneration after injury require highly coordinated complex interplay between resident stem cells and diverse cell types. The function of Dclk1 expressing tuft cells regulating intestinal epithelial DNA damage response for cell survival/self-renewal after radiation-induced injury is unclear. Intestinal epithelial cells (IECs) were isolated and purified and utilized for experimental analysis. We found that small intestinal crypts of Villin(Cre);Dclk1(f/f) mice were hypoplastic and more apoptotic 24 h post-total body irradiation, a time when stem cell survival is p53-independent...
November 23, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27871306/akirin2-is-essential-for-the-formation-of-the-cerebral-cortex
#9
Peter J Bosch, Leah C Fuller, Carolyn M Sleeth, Joshua A Weiner
BACKGROUND: The proper spatial and temporal regulation of dorsal telencephalic progenitor behavior is a prerequisite for the formation of the highly-organized, six-layered cerebral cortex. Premature differentiation of cells, disruption of cell cycle timing, excessive apoptosis, and/or incorrect neuronal migration signals can have devastating effects, resulting in a number of neurodevelopmental disorders involving microcephaly and/or lissencephaly. Though genes encoding many key players in cortical development have been identified, our understanding remains incomplete...
November 21, 2016: Neural Development
https://www.readbyqxmd.com/read/27865785/dnmt1-dnmt3a-and-dnmt3b-cooperate-in-photoreceptor-and-outer-plexiform-layer-development-in-the-mammalian-retina
#10
Ratnesh K Singh, Ramya K Mallela, Abigail Hayes, Nicholas R Dunham, Morgan E Hedden, Raymond A Enke, Robert N Fariss, Hal Sternberg, Michael D West, Igor O Nasonkin
Characterizing the role of epigenetic regulation in the mammalian retina is critical for understanding fundamental mechanisms of retinal development and disease. DNA methylation, an epigenetic modifier of genomic DNA, plays an important role in modulating networks of tissue and cell-specific gene expression. However, the impact of DNA methylation during retinal development and homeostasis of retinal neurons remains unclear. Here, we have created a tissue-specific DNA methyltransferase (Dnmt) triple mutant mouse in an effort to characterize the impact of DNA methylation in retinal development and homeostasis...
November 16, 2016: Experimental Eye Research
https://www.readbyqxmd.com/read/27864295/endothelial-cells-produce-bone-morphogenetic-protein-6-required-for-iron-homeostasis-in-mice
#11
Susanna Canali, Kimberly B Zumbrennen-Bullough, Amanda B Core, Chia-Yu Wang, Manfred Nairz, Richard Bouley, Filip K Swirski, Jodie L Babitt
Bone morphogenetic protein (BMP)6 signaling in hepatocytes is a central transcriptional regulator of the iron hormone hepcidin to control systemic iron balance. How iron levels are sensed to regulate hepcidin production is not known, but local induction of liver BMP6 expression by iron is proposed to have a critical role. To identify the cellular source of BMP6 responsible for hepcidin and iron homeostasis regulation, we generated mice with tissue specific ablation of Bmp6 in different liver cell populations and evaluated their iron phenotype...
November 18, 2016: Blood
https://www.readbyqxmd.com/read/27859428/low-p16-ink4a-expression-in-early-passage-human-prostate-basal-epithelial-cells-enables-immortalization-by-telomerase-expression-alone
#12
Mindy Kim Graham, Lorenzo Principessa, Lizamma Antony, Alan K Meeker, John T Isaacs
BACKGROUND: There are two principal senescence barriers that must be overcome to successfully immortalize primary human epithelial cells in culture, stress-induced senescence, and replicative senescence. The p16(INK4a) /retinoblastoma protein (p16/Rb) pathway mediates stress-induced senescence, and is generally upregulated by primary epithelial cells in response to the artificial conditions from tissue culture. Replicative senescence is associated with telomere loss. Following each round of cell division, telomeres progressively shorten...
November 8, 2016: Prostate
https://www.readbyqxmd.com/read/27827827/histone-acetyltransferase-activity-of-mof-is-required-for-adult-but-not-early-fetal-hematopoiesis-in-mice
#13
Daria G Valerio, Haiming Xu, Meghan E Eisold, Carolien M Woolthuis, Tej K Pandita, Scott A Armstrong
K(Lysine) Acetyltransferase 8 (KAT8, also known as MOF) is a histone 4 lysine 16 (H4K16) acetyltransferase and crucial for murine embryogenesis. Lysine acetyltransferases have been shown to regulate various stages of normal hematopoiesis. However, the function of Mof in hematopoietic stem cell (HSC) development has not yet been elucidated. We set out to study the role of MOF in general hematopoiesis by using a Vav1-cre induced conditional murine Mof knockout system, and found that MOF is critical for hematopoietic cell maintenance and HSC engraftment capacity in adult hematopoiesis...
November 8, 2016: Blood
https://www.readbyqxmd.com/read/27823858/ambient-temperature-modulates-the-effects-of-the-prader-willi-syndrome-candidate-gene-snord116-on-energy-homeostasis
#14
Y Qi, L Purtell, M Fu, K Sengmany, K Loh, L Zhang, S Zolotukhin, A Sainsbury, L Campbell, H Herzog
Germline deletion of the Prader-Willi syndrome (PWS) candidate gene Snord116 in mice leads to some classical symptoms of human PWS, notably reductions in body weight, linear growth and bone mass. However, Snord116 deficient mice (Snord116(-/-)) do not develop an obese phenotype despite their increased food intake and the underlying mechanism for that is unknown. We tested the phenotypes of germline Snord116(-/-) as well as neuropeptide Y (NPY) neuron specific Snord116(lox/lox)/NPY(cre/+) mice at 30°C, the thermoneutral temperature of mice, and compared these to previous reports studies conducted at normal room temperature...
October 27, 2016: Neuropeptides
https://www.readbyqxmd.com/read/27798149/menin-plays-a-critical-role-in-the-regulation-of-the-antigen-specific-cd8-t-cell-response-upon-listeria-infection
#15
Takeshi Yamada, Makoto Kanoh, Shogo Nabe, Toshiaki Yasuoka, Junpei Suzuki, Akira Matsumoto, Makoto Kuwahara, Saho Maruyama, Takuya Fujimoto, Ryo Sakisuka, Masaki Yasukawa, Masakatsu Yamashita
Menin, a tumor suppressor protein, is encoded by the MEN1 gene in humans. Certain germinal mutations of MEN1 induce an autosomal-dominant syndrome that is characterized by concurrent parathyroid adenomas and several other tumor types. Although menin is also expressed in hematopoietic lineages, its role in CD8(+) T cells remains unclear. We generated Menin(flox/flox) CD4-Cre (Menin-KO) mice by crossing Menin(flox/flox) mice with CD4-Cre transgenic (Tg) mice to determine the role of menin in CD8(+) T cells. Wild-type (WT) and Menin-KO mice were infected with Listeria monocytogenes expressing OVA to analyze the immune response of Ag-specific CD8(+) T cells...
October 19, 2016: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/27798140/conditional-deletion-of-the-l-type-calcium-channel-cav1-2-in-oligodendrocyte-progenitor-cells-affects-postnatal-myelination-in-mice
#16
Veronica T Cheli, Diara A Santiago González, Tenzing Namgyal Lama, Vilma Spreuer, Vance Handley, Geoffrey G Murphy, Pablo M Paez
: To determine whether L-type voltage-operated Ca(2+) channels (L-VOCCs) are required for oligodendrocyte progenitor cell (OPC) development, we generated an inducible conditional knock-out mouse in which the L-VOCC isoform Cav1.2 was postnatally deleted in NG2-positive OPCs. A significant hypomyelination was found in the brains of the Cav1.2 conditional knock-out (Cav1.2(KO)) mice specifically when the Cav1.2 deletion was induced in OPCs during the first 2 postnatal weeks. A decrease in myelin proteins expression was visible in several brain structures, including the corpus callosum, cortex, and striatum, and the corpus callosum of Cav1...
October 19, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27798138/a-gabaergic-projection-from-the-centromedial-nuclei-of-the-amygdala-to-ventromedial-prefrontal-cortex-modulates-reward-behavior
#17
Dong-Oh Seo, Samuel C Funderburk, Dionnet L Bhatti, Laura E Motard, Dillan Newbold, Kasey S Girven, Jordan G McCall, Michael Krashes, Dennis R Sparta, Michael R Bruchas
: The neural circuitry underlying mammalian reward behaviors involves several distinct nuclei throughout the brain. It is widely accepted that the midbrain dopamine (DA) neurons are critical for the reward-related behaviors. Recent studies have shown that the centromedial nucleus of the amygdala (CeMA) has a distinct role in regulating reward-related behaviors. However, the CeMA and ventromedial PFC (vmPFC) interaction in reward regulation remains poorly understood. Here, we identify and dissect a GABAergic projection that originates in the CeMA and terminates in the vmPFC (VGat-Cre(CeMA-vmPFC)) using viral-vector-mediated, cell-type-specific optogenetic techniques in mice...
October 19, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27797912/brain-glut4-knockout-mice-have-impaired-glucose-tolerance-decreased-insulin-sensitivity-and-impaired-hypoglycemic-counterregulation
#18
Candace M Reno, Erwin C Puente, Zhenyu Sheng, Dorit Daphna-Iken, Adam J Bree, Vanessa H Routh, Barbara B Kahn, Simon J Fisher
Glucose transporter 4 (GLUT4) in muscle and adipose tissue is important in maintaining glucose homeostasis. However, the role of the insulin-responsive GLUT4 in the central nervous system has not been well characterized. To assess its importance, a selective knock-out of brain GLUT4 (BG4KO) was generated by crossing Nestin-Cre mice with GLUT4-floxed mice. BG4KO mice had a 99% reduction in GLUT4 protein expression throughout the brain. Despite normal fed and fasting glycemia, BG4KO mice were glucose intolerant, demonstrated hepatic insulin resistance, and had reduced brain glucose uptake...
October 17, 2016: Diabetes
https://www.readbyqxmd.com/read/27793816/the-transcription-factor-gli2-as-a-downstream-mediator-of-transforming-growth-factor-%C3%AE-induced-fibroblast-activation-in-ssc
#19
Ruifang Liang, Barbora Šumová, Cinzia Cordazzo, Tatjana Mallano, Yun Zhang, Thomas Wohlfahrt, Clara Dees, Andreas Ramming, Dorota Krasowska, Małgorzata Michalska-Jakubus, Oliver Distler, Georg Schett, Ladislav Šenolt, Jörg H W Distler
OBJECTIVES: Hedgehog signalling plays a critical role during the pathogenesis of fibrosis in systemic sclerosis (SSc). Besides canonical hedgehog signalling with smoothened (SMO)-dependent activation of GLI transcription factors, GLI can be activated independently of classical hedgehog ligands and receptors (so-called non-canonical pathways). Here, we aimed to evaluate the role of non-canonical hedgehog signalling in SSc and to test the efficacy of direct GLI inhibitors that target simultaneously canonical and non-canonical hedgehog pathways...
October 28, 2016: Annals of the Rheumatic Diseases
https://www.readbyqxmd.com/read/27792288/survival-of-mature-t-cells-in-the-periphery-is-intrinsically-dependent-on-gimap1-in-mice
#20
Preeta Datta, Louise M C Webb, Inxhina Avdo, John Pascall, Geoffrey W Butcher
An effective immune system depends upon the survival of mature T cells in the periphery. Members of the GIMAP family of GTPases have been proposed to regulate this homeostasis, supported by the paucity of peripheral T cells in rodents deficient for either GIMAP1 or GIMAP5. It is unclear whether this lack of T cells is a consequence of an ontological defect, causing the thymus to generate and export T cells incapable of surviving in the periphery, or whether (alternatively or additionally) mature T cells intrinsically require GIMAP1 for survival...
October 28, 2016: European Journal of Immunology
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