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1 itor, and abolished by TRPM2 knockout (TRPM2-KO).
2 nsory cortex of the mouse model of FXS (Fmr1 KO).
3 nsory cortex of the mouse model of FXS (Fmr1 KO).
4 M2 channel inhibitor, and prevented by TRPM2-KO.
5 ) diet was significantly impaired in betaTFG KO.
6 n crystal diameters in beta-cells of betaTFG KO.
7 ase isoforms [NO-GC1 knockout (KO) or NO-GC2 KO].
9 oped massive albuminuria (controls: 35-fold; KO: 5400-fold versus baseline), hypoalbuminemia, reduced
12 popolysaccharide (LPS) stimulation, and CTSD KO also reduced caspase-3 activation and apoptosis in ac
13 e investigated whether Tric-a gene knockout (KO) alters the single-channel function of skeletal RyR (
17 od between induction of total PP or PP/Trp53 KO and melanoma development indicates that additional ge
19 the LV-wall adhesions between age-grouped PV-KO and wild-type mice, suggesting a delay in microglial
21 pecific Cx43 knockout in mice (Gja1 (adipoq) KO) and by overexpression and knockdown of Cx43 in cultu
22 meostasis in obesity, we fed A2AAR-knockout (KO) and control mice an HFD for 16 wk to initiate HFD-in
24 1(phox) knockout [KO]), iNOS-deficient (iNOS KO), and C57BL/6 wild-type mice were orally infected wit
25 e-N-acetylneuraminic acid hydroxylase (CMAH) KO, and GGTA1/ CMAH /b1,4 N-acetylgalactosaminyl transfe
26 tate receptors (NMDAR) in the NAc core, TLR4.KO animals exhibit a deficit in low-frequency stimulatio
29 ) elicited hyperalgesia in WT but not in MOR KO animals, as well as in both MOR flox and MOR-Nav1.8 s
34 re further validated using CLEC12A knockout (KO) animals wherein EAE disease induction was delayed an
37 offers several advantages over conventional KO approaches and allows for generation of clean CRISPR/
38 (F-actin) is drastically increased in Rictor KO B cells after BCR stimulation through dysregulating t
39 in polymerization with latrunculin in Rictor KO B cells rescues the defects of BCR signaling and B ce
40 a human ApoE knock-in (KI) or ApoE knockout (KO) background, here we show that P301S/E4 mice have sig
41 , we generated Nlrp3-knockin mice on various KO backgrounds including Il1b/Il18-, caspase-1-, caspase
46 atients were screened on GGTA1/CMAH/B4GalNT2 KO cells and a subset with elevated binding was evaluate
47 this study, we generated and analyzed mNEET KO cells and found that in these cells the mitochondrial
48 d from heterozygous Polbeta mouse tissue and KO cells had lower nucleotide incorporation activity.
49 (-) Triacylglycerol concentrations in the NR-KO cells increased immediately following the addition of
50 s partially restored IL-1 signaling in TRAF6 KO cells, but not in TRAF6/Pellino1/Pellino2 triple-KO c
51 s in PM lipid homeostasis observed in E-Syts KO cells, delayed diacylglycerol clearance from the PM a
56 eparan sulfate proteoglycan (HSPG)-knockout (KO) cells by using a clustered regularly interspaced sho
58 in TRAF6/Pellino1/Pellino2 triple-knockout (KO) cells, but not in TRAF6 KO or Pellino1/2 double-KO c
61 58M) ), hESC line expressing no MECP2 (MECP2-KO), congenic pair of wild-type and mutant RTT patient-s
62 ematopoietic DREAM knockout (KO) mice, DREAM KO control and hematopoietic DREAM KO mice showed a sign
63 Tail bleeding time was prolonged in DREAM KO control mice, but not in WT or DREAM bone marrow chim
64 question, heterozygous ERalpha knockout (WT/KO) dams were fed a control breeder chow diet (25% fat)
67 I2 (PGI2, also called prostacyclin) in Cav-1 KO EC, and this PGI2 increase appeared to stimulate cAMP
75 WT), alpha1, 3-galactosyltransferase (GGTA1) KO, GGTA1/ cytidine monophosphate-N-acetylneuraminic aci
76 iveness, we found that Pde11a knockout mice (KO) given 0.4% lithium chow for 3+ weeks exhibit greater
77 MOR KO mice was found in both sexes, in two KO global mutant lines, and for mechanical, heat and col
79 Human kidney cells with Polbeta knockout (KO) had higher endogenous mitochondrial DNA (mtDNA) dama
80 support the use of the newly described STAT2 KO hamster model for evaluation of promising antiviral t
82 rial and ventricular tissue from adult MEF2A KO hearts revealed a striking difference in chamber gene
84 pon DNAJB6 re-introduction into these DNAJB6-KO HEK293T-alpha-syn cells, aggregation is reduced to th
88 ADPH oxidase-deficient (gp91(phox) knockout [KO]), iNOS-deficient (iNOS KO), and C57BL/6 wild-type mi
90 tation of Eukaryotic Orthologous Groups) and KO (KEGG Orthology) in addition to Pfam domains; (iii) i
91 rsely, genetic or shRNA-mediated conditional KO/knockdown of GSK3beta reduced inhibitory phosphorylat
95 e second-generation human genome-wide CRISPR-KO libraries that included at least one of the improveme
97 (GBPs), are downregulated in STING knockout (KO) macrophages infected with Brucella or transfected wi
99 ganese homeostasis, we used Zip14 knock-out (KO) male and female mice to conduct comparative metaboli
101 FD (45% fat) 4 weeks prior to mating with WT/KO males or heterozygous males with an ERalpha DNA-bindi
106 ocytes to 1% of the control level, Podo-GC-A KO mice and control littermates did not differ in BP, GF
109 Brucella DNA colocalizes with AIM2, and AIM2 KO mice are less resistant to B. abortus infection.
111 n the observed osteopenic phenotype of TIEG1 KO mice as well as the known links between TIEG1 express
113 e in achieved systolic BP, AngII-treated APA-KO mice developed a significant rise in albuminuria not
119 ynaptic connectivity of interneurons in Fmr1 KO mice during a critical period of cortical development
127 etween reward and no-reward levers; however, KO mice failed to discriminate based on relative quantit
131 the lungs of M. tuberculosis-infected IL-21R KO mice had increased expression of T cell inhibitory re
136 nd no differences between wild-type and Fmr1 KO mice in overall whisker-evoked activity, though 45% f
138 ensity of MR images from brains of the Zip14 KO mice is indicative of major manganese accumulation.
139 didymal white adipose tissue (eWAT) of PDE3B KO mice on a SvJ129 background, cAMP/protein kinase A (P
145 otypic characterization of unimmunized ALCAM KO mice revealed a reduced expression of BBB junctional
146 Telemetric analysis from conscious Cx36 KO mice revealed higher variance in heart rate and blood
148 ic lymph node cultures from VDR KO and B-VDR KO mice secreted higher IgE ex vivo than wild-type (WT)
149 physiology, because both C57BL/6J and Pde11a KO mice show increased expression of the pro-inflammator
150 We show that muscle cells of syndapin III KO mice show severe reductions of caveolae reminiscent o
151 ce, DREAM KO control and hematopoietic DREAM KO mice showed a significant delay in time to occlusion.
158 metabolomic signature associated with MAT1A-KO mice that also was present in 49% of the patients; ba
167 mory and LTP is dependent upon APP since APP-KO mice were resistant to oAbeta- and oTau-induced defec
168 used, and high salt-fed (ALDO) systemic GC-A KO mice with enhanced phosphorylation of p38 mitogen-act
169 metabolomes of patients with NAFLD and MAT1A-KO mice with steatohepatitis, we identified 2 major subt
170 sults reveal that hungry mice lacking GPR88 (KO mice) were slow to acquire food-reinforced lever pres
171 stently, mGluR-LTD was impaired in calpain-1 KO mice, and the impairment could be rescued by phosphat
172 In contrast to wild-type (WT) and WAVE1 D2-KO mice, cocaine-induced sensitized locomotor behavior w
211 present study, we found that ALCAM knockout (KO) mice developed a more severe myelin oligodendrocyte
212 urons in the barrel cortex of BC1 knock out (KO) mice display larger excitatory postsynaptic currents
217 analysis of tubules isolated from knockout (KO) mice suggested that ClC-K2 is the main basolateral c
218 s study used B cell-specfic Rictor knockout (KO) mice to investigate how Rictor regulates BCR signali
221 from somatosensory cortex of Fmr1 knock-out (KO) mice, a model of Fragile-X Syndrome, to test the E/I
223 control and nonhematopoietic DREAM knockout (KO) mice, DREAM KO control and hematopoietic DREAM KO mi
224 fat diet-induced ER stress using Zip14(-/-) (KO) mice, which exhibit impaired hepatic zinc uptake.
225 onine adenosyltransferase 1a knockout (MAT1A-KO) mice, which have chronically low levels of hepatic S
232 eloid cell-specific Nrp1-knockout (Nrp1(myel-KO)) mice and applied 2 stringent animal models of sepsi
234 ood-lymphatic mixing and lethality of CLEC-2 KO models, but not their hemostatic/thrombotic defect.
239 vention studies using DBA2/J and Nos3 (eNos) KO mouse models of diabetes, TEPP-46 treatment reversed
240 expression was about the same in both WT and KO mouse visceral yolk sac, brain, and spinal column.
242 dence for this problem in the Fmr1-knockout (KO) mouse model of Fragile X syndrome and describe poten
245 r outflow tract, but in the Nkx2-5(+/-)/Sspn(KO) mutant they commonly deviate into the septum even in
246 not have heart defects, but Nkx2-5(+/-)/Sspn(KO) mutants have a higher incidence of muscular VSD than
247 tological analysis of lung lesions from Muc4(ko)/NDL mice revealed a reduced association of dissemina
248 Moreover, isolated cells derived from Muc4(ko)/NDL tumors interact with fewer blood cells when inje
249 eficit in HSP is bidirectional because Mecp2 KO neurons also failed to scale down mEPSC amplitudes an
250 PA-type of glutamate receptors in HSP, Mecp2 KO neurons have lower levels of early endosome antigen 1
252 ation of a molecular deficit in HSP in Mecp2 KO neurons provides potentially novel targets of interve
253 In addition, expression of EEA1 in Mecp2 KO neurons reduced mEPSC amplitudes to wild-type levels,
257 strate that a CRISPR/Cas9-mediated knockout (KO) of a DnaJ protein, DNAJB6, in HEK293T cells expressi
258 f AKT rescued GCB-DLBCL lines from knockout (KO) of the BCR or 2 mediators of tonic BCR signaling, SY
260 ion was combined with either AMPK beta1beta2 KO or alpha2KD, contraction-stimulated glucose transport
263 ot seen in PKR-like ER kinase knockout (PERK-KO) or phosphodeficient eukaryotic translation initiatio
264 on knocked in (WT/KI) to produce WT, ERalpha KO, or ERalpha KIKO females lacking ERE-dependent ERalph
265 ed aberrant Tuj1(+) neuronal migration in RB-KO organoids and upregulation of the gene encoding VLDLR
267 al transplant patients to 3 glycan knockout (KO) pig cells and class I swine leukocyte antigens (SLA)
268 -acetylgalactosaminyl transferase (B4GalNT2) KO pigs were screened for human antibody binding using f
270 te the marked reduction of GC-A mRNA in GC-A KO podocytes to 1% of the control level, Podo-GC-A KO mi
271 is sufficient to cause the apneas in Necdin-KO pups, and that fluoxetine may offer therapeutic benef
278 as no change in mitochondrial content in the KO rats, maximal ADP-stimulated respiration was higher i
282 mune responses are normal in Kv1.3 knockout (KO) rats, suggesting that KCa3.1 can compensate for the
284 III is crucial for caveolar invagination and KO rendered the cells sensitive to membrane tensions.
286 xpression of AtGET3a in a receptor knockout (KO) results in severe growth defects, suggesting presenc
287 er genes, leading to premature senescence of KO siliques, whereas RCS and senescence marker levels in
288 of CLEC-2 in vivo have focused on knockout (KO) studies in which both the receptor and its signaling
293 ed ectopically localized Tuj1(+) cells in RB-KO teratomas grown in vivo Taken together, these results
294 n rates of MG cells derived from betaENaC MG KO than control mice, suggesting that betaENaC plays a r
295 revealed smaller beta-cell masses in betaTFG KO than in controls, likely attributable to diminished b
296 reduced only at 1 h, whereas in the complete KO, this effect also included the late disease phase (8
300 ine embryos lacking EPH receptor A4 (Epha4KO/KO), which is upstream of alpha2-chimaerin in corticospi
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