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1 gous for either CR1(long), CR1(short) or CR1(KO).
2 the observed metabolic phenotype of EC-AGO1-KO.
7 innate lymphoid (Il2rg knockout mice [Il2rg (KO)]), adaptive immune (Rag1 knockout mice [Rag1 (KO)]),
11 lysis demonstrated blood from platelet-COX-1-ko and global-COX-1-ko mice produced similar eicosanoid
12 ype switching, since both PIV-vaccinated B2m KO and MHC-II KO mice produced less Coxiella-specific Ig
15 ipoma cell line 621-101, MITF knockout (MITF.KO) and MITF-A overexpressing (MITF.OE) cell lines were
18 el in mice with (WT) or without Lgals2 (Gal2-KO) and showed that Gal2 deficiency ameliorated DSS-indu
20 ( KO) ) or Toll-like receptor 4 (TLR4; TLR4( KO) ), and animals were fed an HFD or treated with lipop
21 ice with EC-AGO1 deletion (EC-AGO1-knockout [KO]) and their wild-type littermates to a fast food-mimi
23 ate cancer cells in WT and apolipoprotein-AI KO (apoA1-KO) C57BL/6J mice revealed that WT hosts, cont
25 were as many vesicles in lobule V of CB (1) -KO as in CB (1) -WT, but their distribution decreased dr
26 When testing the effects of inducible EphA4 KO at different timepoints in SOD1(G93A) mice, we found
29 ause of its active utilization by the aralar-KO brain and the likely involvement of neuronal NAA in p
35 cells in WT and apolipoprotein-AI KO (apoA1-KO) C57BL/6J mice revealed that WT hosts, containing hig
36 ing and HF hearts, 4 mouse lines: wild-type, KO (CaMKIIdelta-knockout), CaMKIIdeltaC transgenic in wi
41 thermore, overexpression of PYCR1 in PINCH-1 KO cells restores proline synthesis and cell proliferati
42 y a drop in TET2 levels, yet the analysis of KO cells suggested that TET2 is responsible for most 5fC
43 5) The disappearance of some proteins in 2-KO cells took place despite up-regulation of their mRNAs
47 in the MITF.OE cells and reduced in the MITF.KO cells, and luciferase assays showed this was due to t
48 k2 at tyrosine 402 is decreased in NK92 CD56-KO cells, demonstrating a functional link between CD56 a
50 ists reacidify lysosomes in PSEN1 Knock out (KO) cells and fibroblasts from PSEN1 familial AD patient
51 reted proteins upregulated in Ocy454-Gsalpha(KO) cells compared to Ocy454-Gsalpha(cont) , whereas sem
52 of CM from Ocy454 Gsalpha(cont) and Gsalpha(KO) cells identified neuropilin-1 (Nrp-1) and granulin (
55 knockdown of Nrp-1 and Grn in Ocy454-Gsalpha(KO) cells partially rescued the inhibition of osteoclast
58 anged expression of 114 proteins while Keap1-KO changed expression of 117 proteins with 10 proteins i
59 d as the basal function of Nrf2, while Keap1 KO-changed proteins are involved in cellular detoxificat
60 Gene ontology analysis suggested that Nrf2 KO-changed proteins are involved in metabolism of oxidor
61 also reduced in double Hfe/endothelial Bmp2 KO compared with single endothelial Bmp2 KO female mice.
64 (KO) mice, reduced by 92% in Chk;Csk double KO (DKO) mice, and partially rescued in Chk;Csk;Ptprj tr
68 on defects were created in Ank knockout (Ank KO), Enpp1 mutant (Enpp1(asj/asj)), and double KO (dKO)
69 Together, the larger, faster EPSCs in the KO explain the altered complex spike responses, which de
70 e used a forebrain neuron-specific aromatase KO (FBN-ARO-KO) mouse model to deplete neuron-derived E2
72 laque abundance was elevated in PS2APP;Trem2(ko) females at 6-7 months; but by 12 or 19-22 months of
74 pletion of mitochondrial CoQ within the Fmr1 KO forebrain closed the channel, blocked the pathologica
76 ver CC1 null mutation augmented IRI-OLT (CC1-KO->WT) by enhancing ROS expression and HMGB1 translocat
77 ROS induction, and HMGB1 translocation (CC1-KO->WT), whereas ASK1 silencing (siRNA) promoted cytopro
78 ide (CyP) immunosuppressed or RAG2 knockout (KO) hamsters were exposed to severe acute respiratory sy
80 of caspases 3 and 7 in TTC7A-knockout (TTC7A-KO) HAP1 (human haploid) cells and reduce the susceptibi
85 l response to HuNoVs, we developed knockout (KO) HIE lines for IFN alpha and lambda receptors and the
87 L-cholesterol, grew larger tumors than apoA1-KO hosts with lower levels of total and HDL-cholesterol.
89 marrow chimera mice demonstrated that STAT6 KO in either the CNS or periphery exacerbated ICH outcom
92 MNTB (and compensate for each other in each KO); in contrast, LSO neurons require Kv3.3 subunits for
93 ly inhibited cell proliferation, while SSTR1 KO induced cell proliferation, thus suggesting that HRH1
96 e total liver BA levels were similar between KO/KD and KO, there was significant dysregulation of BA
98 Although hepatocyte junctions were intact, KO/KD livers had significant canalicular defects, which
100 was higher in PIP2;5 OE and lower in pip2;5 KO lines compared with the corresponding wild-type plant
104 te immune gene expression in Lrrk2 knockout (KO) macrophages is driven by a combination of mitochondr
105 loped more atherosclerotic lesions than Apoe KO male controls, regardless of diet (standard or WTD).
106 idal neurons in astrocyte-specific ephrin-B1 KO male mice, which coincided with a greater vGlut1/PSD9
110 ls are increased in FXR-knockout (KO) or SHP-KO mice and are decreased by activation of FXR in a SHP-
111 e, we report the characterizations of Mfsd7c-KO mice and compare these characterizations to phenotypi
112 obtained from striated muscle-specific Speg-KO mice and compared them with wild-type (WT) controls.
113 vealed a complete lack of testosterone in XY-KO mice and marked accumulation of progesterone in XX-KO
114 n was observed in colonoids derived from DRA-KO mice and short hairpin RNA-mediated DRA knockdown in
117 nges were remarkably reduced in Ins2 (Akita)/KO mice and, likewise, in vitro experiments with XBP1 si
118 lar bone formation between WT and Col6alpha2-KO mice based on the mineral appositional rate, bone for
120 ever, the gross levels of H3R17me2a in CARM1 KO mice did not significantly decrease, indicating that
121 Knockout (KO) of IL-6 in muscle lamin A/C-KO mice diminishes the deficits in trabecular bone mass
122 rebrain glutamatergic neuron-selective Ahnak KO mice display a depression-like behavioral phenotype s
124 Eight-week-old double endothelial Bmp6/Bmp2 KO mice exhibited a similar degree of hepcidin deficienc
125 onstrated that ovariectomized female FBN-ARO-KO mice exhibited significantly attenuated astrocyte act
131 r of NGAL-deficient CD4(+) T cells from NGAL KO mice into CD4 KO or WT mice led to worse renal functi
132 We show that the auditory synapse of GLAST KO mice is more vulnerable to cisplatin administration d
134 investigated conditional/conventional double KO mice of BMP-receptor 1a (BMPR1a; targeted to PV-INs)
137 since both PIV-vaccinated B2m KO and MHC-II KO mice produced less Coxiella-specific IgG than PIV-vac
139 lood from platelet-COX-1-ko and global-COX-1-ko mice produced similar eicosanoid profiles in vitro: f
142 Atherosclerotic plaques from HFD-treated KO mice showed increased infiltration of M1 type inflamm
143 vel multiple feature selection tools in Fmr1-KO mice to provide direct evidence that normal functioni
145 , the total chymotrypsinogen content in Ctrl-KO mice was barely reduced indicating that CTRL is a low
146 e response to skeletal muscle injury in Speg-KO mice was compared with that of WT mice, leading to th
149 tation of IP-mediated relaxation, iSM-Gprc5b-KO mice were protected from arterial hypertension, and t
152 B signalling was disrupted in the OC of Nhe6 KO mice, probably due to TrkB reduction, caused by over
153 ed on the enhanced memory phenotype of Tiam1 KO mice, Tiam1 may be a potential target for the treatme
156 mice, rats, and NHPs, but not in M(1) mAChR KO mice, VU0453595 produced dose-related increases in hi
157 flammation and cognitive impairment in NLRP3-KO mice, we transplanted VAT from obese WT or NLRP3-KO d
158 WT) B6 mice, the symptomatic corneas of CD1d KO mice, which lack iNKT cells, showed (i) decreases in
159 he subcutaneous and brown adipose tissues of KO mice, with greater vascularity and enhanced browning
192 Lung tumor suppressor gene Gprc5a-knockout (ko) mice are susceptible to lung inflammation, tumorigen
194 ccinated WT mice to naive CD4-deficient (CD4 KO) mice demonstrated that antigen-experienced CD4(+) T
195 3 months of infection with H felis, Nlrc5(mo-KO) mice developed gastric hyperplasia (P < .0001), sple
197 ere delayed in only the PVPV-Akt1 knock out (KO) mice in association with increased apoptosis with no
199 cking either IL-12 or IFNgamma in Tnfaip3(Lg-KO) mice restored Th2 responses, whereas administration
200 d amyloid precursor protein (APP) knock-out (KO) mice to assess the effects of Abetaos on glutamaterg
201 We generated ZO-1 CM-specific knockout (KO) mice using alpha-Myosin Heavy Chain-nuclear Cre (ZO-
202 In this study, we found that IRF3-knockout (KO) mice were greatly protected from sepsis in a clinica
204 his study, we found that Opn3-knockout (Opn3-KO) mice were prone to diet-induced obesity and insulin
206 ice using Lgr5-regulated CRE-ERT2 (Lkb1(Lgr5-KO) mice) and the traced lineages by using a CRE-depende
207 rotein (Gsalpha) in osteocytes (Dmp1-Gsalpha(KO) mice) have abnormal myelopoiesis, osteopenia, and re
209 gile X Mental Retardation 1 (Fmr1) knockout (KO) mice, a model of Fragile X Syndrome (FXS) with abrog
210 Platelet count was normal in Chk knockout (KO) mice, reduced by 92% in Chk;Csk double KO (DKO) mice
214 we suppressed beta-catenin in Mdr2 knockout (KO) mice, which develop sclerosing cholangitis due to re
216 ed Na(v) availability in Fhf2 knockout (Fhf2(KO)) mice predisposes to abnormal excitability at the ti
217 FD feeding of CysC-deficient (CysC knockout [KO]) mice worsened obesity-associated adipose tissue inf
218 espiration due to futile proton leak in Fmr1 KO mitochondria caused by coenzyme Q (CoQ) deficiency an
219 ameliorates ER stress and fibrosis in Grp78 KO mouse and IPF lung slice cultures.Conclusions: These
220 ogenesis machinery, in mitochondria from TAZ-KO mouse cells and in CL-deleted yeast crd1Delta cells,
221 P1 with occludin and E-cadherin genes in DRA-KO mouse colon, suggesting that posttranscriptional mech
222 in tRNA were significantly decreased in Tet2 KO mouse embryonic stem cells (mESCs) in comparison with
225 g a pan-brain-specific conditional knockout (KO) mouse incapable of FAO due to the loss of carnitine
226 ebrain neuron-specific aromatase KO (FBN-ARO-KO) mouse model to deplete neuron-derived E2 in the fore
232 content, and function of lysosomes in PARK2 KO neurons and reveal an important new connection betwee
234 ort that betaOHB efficiently recovers aralar-KO neurons from deficits in basal-stimulated and glutama
237 while, conversely, mice with liver-specific KO of Arrdc3 (L-Arrdc3 KO) have increased IR protein in
241 Here, we induced a CRISPR/Cas9-mediated KO of the TCRbeta chain in combination with a second-gen
246 Mice with a Purkinje-cell-specific knockout (KO) of the calcium-activated K+ channel SK2 (L7-SK2) sho
248 uch cells to investigate the impact of PARK2 KO on the lysosomal compartment and found a clear link b
249 nt CD4(+) T cells from NGAL KO mice into CD4 KO or WT mice led to worse renal function than transfer
250 iR-802 levels are increased in FXR-knockout (KO) or SHP-KO mice and are decreased by activation of FX
251 hage/monocyte-specific deletion of YAP (YAP( KO) ) or Toll-like receptor 4 (TLR4; TLR4( KO) ), and an
253 , adaptive immune (Rag1 knockout mice [Rag1 (KO)]), or both systems (Il2rg (KO)/Rag1 (KO)), were empl
258 and restitution led to worsening of the Mdr2 KO phenotype, suggesting caution in targeting beta-caten
263 t mice [Rag1 (KO)]), or both systems (Il2rg (KO)/Rag1 (KO)), were employed to investigate their respe
264 ) juveniles, the Il2rg (KO)/Tg(+) and Il2rg (KO)/Rag1 (KO)/Tg(+) juveniles exhibited suppressed expre
265 present a detailed phenotyping of the TRPA1 KO rat in models of pain, itch, and asthma that have pre
266 PA1 activation, we have found that the TRPA1 KO rat shows apparently normal behavioral responses in m
269 species and demonstrate the utility of Fmr1-KO rats for investigating drugs for the treatment of FXS
271 examined Fmr1-targeted transgenic rats (Fmr1-KO rats) as an alternative preclinical model of FXS.
276 opy reveals that many disc membranes in Prcd-KO rod photoreceptor neurons are irregular, containing f
279 1 were knocked out by CRISPR, HRH1 knockout (KO) significantly inhibited cell proliferation, while SS
280 ng syngeneic SR-B1 WT (SR-B1(+/+)) and SR-B1 KO (SR-B1(-/-)) prostate cancer cells in WT and apolipop
281 that Rhbdf1 responds differently to distinct KO strategies, for example, by skipping exons and reinit
285 +) and Rag1 (KO)/Tg(+) juveniles, the Il2rg (KO)/Tg(+) and Il2rg (KO)/Rag1 (KO)/Tg(+) juveniles exhib
286 s, the Il2rg (KO)/Tg(+) and Il2rg (KO)/Rag1 (KO)/Tg(+) juveniles exhibited suppressed expression leve
287 between the immunocompetent Tg(+) and Rag1 (KO)/Tg(+) juveniles, the Il2rg (KO)/Tg(+) and Il2rg (KO)
288 with IL-33(HET)/Tg+ mice, although the IL-33(KO)/Tg+ mice had significantly reduced levels of MUC5AC
289 ly in the distal intestine of VDR null mice (KO/TG mice) results in the normalization of serum calciu
290 ver BA levels were similar between KO/KD and KO, there was significant dysregulation of BA transporte
293 e, tyramine accumulation was higher in TAAR1-KO versus wild-type mice, suggesting a negative feedback
294 lammatory/immune network was similar in IRF3-KO versus WT septic mice, although the tempo of connecti
298 g1 (KO)]), or both systems (Il2rg (KO)/Rag1 (KO)), were employed to investigate their respective cont