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1 xytamoxifen (OHT) into agonists in the AF2ER knock-in mouse.
2  hyperresponsiveness in the hGX-sPLA(2)(+/+) knock-in mouse.
3 he circadian clock using PERIOD2 (PER2)::LUC knock-in mouse.
4 oped a Runx1-green fluorescent protein (GFP) knock-in mouse.
5 cortical neurons derived from the PS-1 P264L knock-in mouse.
6 alpha loss-of-function phenotype of the C43S knock-in mouse.
7 pileptic encephalopathy, the Gabrg2(+/Q390X) knock-in mouse.
8 he generation of a floxed GFP-C5aR1 reporter knock-in mouse.
9               Here, we show that the genetic knock-in mouse and human variant allele carriers exhibit
10 alization in OSNs, we generated a SLP3(eGFP) knock-in mouse and imaged the apical epithelium, includi
11                                 Using a lacZ/knock-in mouse and three lines of transgenic mouse harbo
12 rmed these findings in an analogous V region knock-in mouse and/or in non-Tg mice.
13                           Using the Ptc-LacZ knock-in mouse as a second Gli responsive reporter, we s
14                      Use of an En-1/tau-LacZ knock-in mouse as an autonomous marker for these neurons
15 y source of inherited instability in the Hdh knock-in mouse, as it is in man, but that the underlying
16  chain rearrangements in an anti-DNA H chain knock-in mouse, B6.56R.
17 ologous recombination was used to generate a knock-in mouse bearing the RyR2-V2475F mutation.
18 s associate with mitochondria in Hdh(CAG)150 knock-in mouse brain and that this association increases
19 aptosomal fraction isolated from Hdh(CAG)150 knock-in mouse brain.
20  BDNF release and early neuropathology in HD knock-in mouse brain.
21 ted the repeat expansion in the variant SCA3 knock-in mouse by cell-type specific Cre/LoxP recombinat
22 e LxCxE domain in vivo, we have generated a "knock-in" mouse by replacing the wild-type cyclin D1 gen
23         We used gene targeting to generate a knock-in mouse carrying a null allele of enamelin (Enam)
24                               We generated a knock-in mouse carrying the disease-associated mutation
25                               The homozygous knock-in mouse carrying the missense P448L mutation almo
26 thways downstream of NOD2, we created a Nod2 knock-in mouse carrying the most common mutation seen in
27 cultured hippocampal neurons from a DeltaPIX knock-in mouse, CDI is absent.
28 lished in p53(QS) (Leu25Trp26 to Gln25Ser26) knock-in mouse cells after DNA damage, to determine the
29                               A "redox-dead" knock-in mouse containing a C43S mutation exhibits pheno
30                       Finally, using a novel knock-in mouse containing Cx43-MK4A mutation, we show in
31 across an allelic series of heterozygous CAG knock-in mouse embryonic stem (ES) cell lines (Hdh(Q20/7
32 37Q knock-in mice, and found that homozygous knock-in mouse embryos were typically small in size and
33                                     In R137Q knock-in mouse embryos, the BER efficiency was severely
34 (wild-type) and Hdh(Q111) (mutant huntingtin knock-in) mouse embryos.
35 raction, we generated an EPCR point mutation knock-in mouse (EPCR(R84A/R84A)) which lacks the ability
36                        Hence, we generated a knock-in mouse expressing a hemagglutinin (HA)-epitope-t
37  after antigenic stimulation, we generated a knock-in mouse expressing a modified form of the Cameleo
38             We subsequently generated an HAQ knock-in mouse expressing a mouse equivalent of the HAQ
39                        A new study reports a knock-in mouse expressing an identical mutation, bridgin
40 rons in acute sagittal brain slices from the knock-in mouse expressing epitope-tagged DAT.
41 nal distribution of DAT using the transgenic knock-in mouse expressing hemagglutinin (HA) epitope-tag
42 ood pressure control in vivo, we generated a knock-in mouse expressing only a C42S 'redox-dead' versi
43                          ECs isolated from a knock-in mouse expressing p27(Kip1) with a mutation of t
44 ossing Pten conditional knockout mice with a knock-in mouse expressing the Cre recombinase in the CD4
45                                Cells from a "knock-in" mouse expressing a NF-kappaB p65 mutant bearin
46 armacoperone drug in a small animal model, a knock-in mouse, expressing a mutant GnRHR.
47 ent protein (GFP) in Arf(+/GFP) heterozygous knock-in mouse eyes.
48 y macrophages from a Zfp36-V5 epitope tagged knock-in mouse generated by CRISPR/Cas9-mediated genome
49                         We discovered that a knock-in mouse harboring a mutated thyroid hormone recep
50  collagen expression in vivo, we generated a knock-in mouse harboring a mutation that abolished the s
51     We generated the first patient-mimicking knock-in mouse harbouring the most common disease-causin
52                               We generated a knock-in mouse in which a single amino acid residue, whi
53 e of these functions in vivo, we generated a knock-in mouse in which four amino acid substitutions in
54             1337-1344) describe a mutant p53 knock-in mouse in which normal tissues and some tumors h
55                               We generated a knock-in mouse in which the endogenous H19/Igf2 ICR (mIC
56 nologic tolerance mechanisms, we generated a knock-in mouse in which the Ig heavy chain (HC) variable
57             In this study, using a TCR alpha knock-in mouse in which the knock-in alpha-chain can be
58 their importance for inhibition we created a knock-in mouse in which these residues are replaced by p
59  present study was to develop an NPC1 I1061T knock-in mouse in which to test proteostatic therapies.
60 of IL-23 in vivo, we have generated a novel "knock-in" mouse in which we have replaced the intracellu
61 se MPNs, we generated an inducible Jak2V617F knock-in mouse, in which the expression of Jak2V617F is
62                              The Hdh(CAG)150 knock-in mouse is a valid model to evaluate early events
63    The early motor phenotype observed in the knock-in mouse is reminiscent of repetitive movements of
64 o test this directly in vivo, we generated a knock-in mouse lacking the last seven residues of GluR1,
65                                            A knock-in mouse lacking the midregion, NLS, and C terminu
66                                 Using a PTEN knock-in mouse lacking the PDZ motif, and a cell-permeab
67 ineered a del595-612 PGHS-2 (Delta 18 COX-2) knock-in mouse lacking this 18-amino acid segment.
68             We further created an SHOX/Shox2 knock-in mouse line (replacement of Shox2 with SHOX, ref
69 f this study was to characterize a Krt12-Cre knock-in mouse line for corneal epithelium-specific gene
70                         Here, we generated a knock-in mouse line in which CB1-expressing neurons expr
71 ithin the DR in the current study, we used a knock-in mouse line in which expression of green fluores
72 c inducible fate mapping using a Gbx2(CreER) knock-in mouse line that descendants of Gbx2(+) cells as
73                                  We report a knock-in mouse line that expresses the isogenetic mutati
74 or Exclusively Activated by a Designer Drug) knock-in mouse line to manipulate intracellular Ca(2+) l
75                               We generated a knock-in mouse line with an MS2 binding site (MBS) casse
76  hypothesis directly in vivo, we generated a knock-in mouse line with targeted mutation of the Ca(v)b
77           Here we characterized a Sox2-CreER knock-in mouse line with two independent reporter mouse
78 essing neurons, we generated a HS3ST-2-hPLAP knock-in mouse line, in which HS3ST-2-expressing neurons
79 ng a gene targeting approach, we generated a knock-in mouse line, in which N-terminal hemagglutinin e
80 rs and defects in spindle orientation in our knock-in mouse line, which are absent in knockout animal
81 ating tissues, we engineered a Smarca4(FLAG) knock-in mouse line.
82            Here we present a toolbox of four knock-in mouse lines engineered for strong, Cre-dependen
83 ic changes in other organs, we generated two knock-in mouse lines on the C57BL/6N background harborin
84 such phenotypes, we have generated Hdh(Q111) knock-in mouse lines that are congenic for C57BL/6, FVB/
85                                          Two knock-in mouse lines that differ in the integration site
86 ddress these issues, we studied three Mrgprd knock-in mouse lines using an ex vivo somatosensory prep
87                                      Using a knock in mouse model with a Ser312 to Ala mutation, we s
88 units in the homozygous calsequestrin 2-R33Q knock-in mouse model (R33Q) R33Q knock-in mouse model.
89   Furthermore, we created a FIP200-4A mutant knock-in mouse model and found that specifically blockin
90 ncy and mutation frequency, we established a knock-in mouse model by inserting a core Sgamma1 region
91 lopment of leukemia, we generated a FLT3/ITD knock-in mouse model by inserting an ITD mutation into t
92                                            A knock-in mouse model carrying the homologous p.Tyr97Cys
93 e the roots of this phenomenon, we created a knock-in mouse model carrying the mutation associated wi
94                                            A knock-in mouse model carrying the patient mutation p.Asn
95                                 We created a knock-in mouse model containing a potent dominant negati
96 mplications of PTMs on SRC-3, we developed a knock-in mouse model containing mutations at four conser
97                                         This knock-in mouse model enabled the use of a highly potent
98 yR2 in living cardiomyocytes, we generated a knock-in mouse model expressing a GFP-tagged RyR2 (GFP-R
99 p53 was further validated in vivo by using a knock-in mouse model expressing an acetylation-mimicking
100                                    We used a knock-in mouse model expressing the ACTA1 His40Tyr actin
101                          Here we introduce a knock-in mouse model expressing the Atg16L1 T300A varian
102                      We have characterized a knock-in mouse model expressing this dominant gain-of-fu
103           To our knowledge this is the first knock-in mouse model for a crystallin mutation causing h
104 n this study, we report the development of a knock-in mouse model for breast cancer where the endogen
105                           Here we describe a knock-in mouse model for Cre-loxP-based conditional expr
106 ment and progression, we took advantage of a knock-in mouse model harboring a mutation in the Thrb ge
107                               We generated a knock-in mouse model harboring the c.365 G>C Fhl1 mutati
108 s, we took advantage of a recently generated knock-in mouse model in which an axonal tracer, farnesyl
109 gic dysplasia and BM hyper-cellularity, in a knock-in mouse model in which cyclin E mutations were in
110                 Here we demonstrate, using a knock-in mouse model in which GFRalpha1 is no longer loc
111                We have generated an FLT3/ITD knock-in mouse model in which mice with an FLT3/ITD muta
112                     Here we describe a novel knock-in mouse model in which the prerearranged IgH locu
113        To address this, we generated a Brca2 knock-in mouse model lacking exons 4-7 and demonstrated
114     To address this, we generated a germline knock-in mouse model of cytoplasm-predominant Pten and c
115  study used a transgenic Col8a2(Q455K/Q455K) knock-in mouse model of early-onset FECD to identify the
116 nt these issues, we have studied a JAK2V617F knock-in mouse model of ET in which all megakaryocytes a
117          To our knowledge, this is the first knock-in mouse model of HD to show increased glial fibri
118                      We have developed a new knock-in mouse model of HD with a chimeric mouse/human e
119 d the synaptic connectivity in a full-length knock-in mouse model of HD, the zQ175 mouse.
120 ies CAG length-dependent phenotypes in a Htt-knock-in mouse model of HD.
121                  We developed a CaV1.1-R528H knock-in mouse model of hypokalaemic periodic paralysis
122 these limitations, we generated an inducible knock-in mouse model of iRFP713.
123 ter understand these defects, we generated a knock-in mouse model of l-DOPA-responsive dystonia (DRD)
124  and early cone degeneration in the mutation knock-in mouse model of LCA.
125                       We aimed to generate a knock-in mouse model of odontohypophosphatasia with a pr
126                          We have developed a knock-in mouse model of OPMD (Pabpn1+/A17) that contains
127 ore, EndMT is an early event in a JAK2-V617F knock-in mouse model of primary myelofibrosis.
128                                      Using a knock-in mouse model of SCA1 that recapitulates the sele
129 rived embryonic stem (ES) cells from a novel knock-in mouse model of SCD and tested a protocol for co
130 glutamine AR formed in cell culture and in a knock-in mouse model of spinal and bulbar muscular atrop
131 d the pattern of CAG repeat instability in a knock-in mouse model of spinocerebellar ataxia type 1 (S
132                                      Using a knock-in mouse model of the FAAH polymorphism that contr
133 investigate this question, we utilized a CGG knock-in mouse model of the Fragile X premutation with 1
134  of adult-born neurons, we developed a novel knock-in mouse model that allowed us to specifically and
135              MW-151 was tested in an APP/PS1 knock-in mouse model that exhibits increases in AD-relev
136               Here, we characterized a novel knock-in mouse model that expresses mouse HD gene homolo
137 bellar ataxia 17, we generated a conditional knock-in mouse model that expresses one copy of the muta
138       Here, we generated a double homozygous knock-in mouse model that incorporates the Swedish famil
139                                      Using a knock-in mouse model that recapitulates the clinical fea
140                          Here, we describe a knock-in mouse model that reproduces the testicular atro
141                                         This knock-in mouse model thus links the ability of E2F1 to d
142 inal DNA-binding domain and also generated a knock-in mouse model to analyze the physiological signif
143        In this study we generated a Cbfb-GFP knock-in mouse model to characterize the normal expressi
144 n this study, we used the gp130(F/F) (Il6st) knock-in mouse model to examine the pathogenic contribut
145 ze et al use a tetracycline-inducible Dnmt3b knock-in mouse model to investigate how DNMT3B-mediated
146 a Neurog3-enhanced green fluorescent protein knock-in mouse model to isolate endocrine progenitor cel
147                                     A LGMD2I knock-in mouse model was generated to express the most f
148 f this E2F1 phosphorylation event in vivo, a knock-in mouse model was generated, in which serine 29 w
149                                      Using a knock-in mouse model where the sequence for the enhanced
150 independent effects of SSRIs, we developed a knock-in mouse model whereby high-affinity interactions
151 s prognostic difference, we have generated a knock-in mouse model with a D838Y point mutation in FLT3
152                          We have generated a knock-in mouse model with a homozygous Lig4 R278H mutati
153                                 We created a knock-in mouse model with an RNase H2 AGS mutation in a
154 role in disease pathogenesis, we generated a knock-in mouse model with NB disruption mediated by 2 po
155                               We generated a knock-in mouse model with the 5-bp deletion in the Elovl
156 thogenesis of this condition, we generated a knock-in mouse model with this mutation.
157      We generated a novel Shank3 conditional knock-in mouse model, and show that re-expression of the
158 sis on these biochemical changes utilizing a knock-in mouse model, RMOR, in which MORs undergo morphi
159 sorders and profound deafness, and studied a knock-in mouse model, Ush1c c.216G>A, for Usher syndrome
160   In a phosphorylation-competent p300(G442S) knock-in mouse model, we demonstrate that HGP is now exq
161      Using a transgenic Gpr54-null IRES-LacZ knock-in mouse model, we demonstrate that neurons contai
162                                 Using a Hras knock-in mouse model, we demonstrate that specificity fo
163                          Using a conditional knock-in mouse model, we show that endogenous expression
164 trin 2-R33Q knock-in mouse model (R33Q) R33Q knock-in mouse model.
165  in vivo properties of this mutant in a gene knock-in mouse model.
166 eta-SMMHC was further confirmed in vivo in a knock-in mouse model.
167 thylation levels in a tetracycline-inducible knock-in mouse model.
168  vector to express IVS-AAA in the brain of a knock-in mouse model.
169 veral adult tissues using a novel Tcf3-CreER knock-in mouse model.
170  in vivo using a novel Ncc T58M (human T60M) knock-in mouse model.
171 activity were normal in the whole lung of a "knock-in" mouse model carrying an S32T mutation in the P
172                   We have generated an R98C 'knock-in' mouse model of Charcot-Marie-Tooth type 1B, wh
173  gene-knock-in (A2BAR-knockout/reporter gene-knock-in) mouse model and showed receptor gene expressio
174 esis, we created a site-directed transgenic (knock-in) mouse model carrying a conditional MN1-TEL tra
175 ocampal neurons from a premutation (Fmr1 CGG knock-in) mouse model revealed impaired development of e
176  CGG-repeat length in a congenic (CGG-repeat knock-in) mouse model using 57 wild-type and 97 expanded
177 al neurogenesis in Huntington's disease (HD) knock-in mouse models and associated embryonic stem cell
178 ECD) using two alpha2 collagen VIII (Col8a2) knock-in mouse models and human FECD tissues.
179                   Transgenic, knock-out, and knock-in mouse models and their intercrosses are more re
180                 Therefore, we generated cTnI knock-in mouse models carrying an R21C mutation to evalu
181 e pre-B cell lines and later demonstrated in knock-in mouse models carrying immunoglobulin heavy chai
182 evelopment in vivo, we generated conditional knock-in mouse models in which the granulosa cells expre
183 ts cellular sources, we generated human apoE knock-in mouse models in which the human APOE gene is co
184               Here we show, using homozygous knock-in mouse models in which we replace murine Mc3r wi
185 to different backgrounds and/or new knockout/knock-in mouse models is often time-consuming (6 months
186 e STN was studied in BAC transgenic and Q175 knock-in mouse models of HD.
187 l to CAG repeat length and is present in all knock-in mouse models of Huntington's disease (HD) with
188 r phenotypes in the striatum of six distinct knock-in mouse models of the HD mutation.
189 sq2 derived from gene-targeted knock-out and knock-in mouse models that have recently become availabl
190                          We have created two knock-in mouse models to study the mechanisms that regul
191 etermine the in vivo role of Ser571, 2 Scn5a knock-in mouse models were generated expressing either:
192 tant ras transgenes, conditionally expressed knock-in mouse models, and somatic cell knockout of muta
193 h Tbx18(LacZ), Tbx18(H2BGFP), and Tbx18(Cre) knock-in mouse models, we demonstrate LacZ and H2BGFP (n
194                                Using two Igh knock-in mouse models, we found that RNA polymerase II a
195                   Using humanized p53-mutant knock-in mouse models, we have identified a gain of onco
196 ion sites in IDH1 and IDH2 using conditional knock-in mouse models.
197                          We include two SCA3 knock-in mouse models: our previously published model th
198                                       Using "knock-in" mouse models expressing mutant EpoRs, we found
199         By using primary CTLs derived from a knock-in mouse of the CG membrane protein Synaptobrevin2
200 uman signal regulatory protein alpha (SIRPA) knock-in mouse on a Rag2(-/-) Il2rg(-/-) background (SRG
201 phorylation of the RyR at serine 2808 with a knock-in mouse prevented the decrease in spark-to-spark
202 phorylation of the RyR at serine 2808 with a knock-in mouse prevented the decrease in spark-to-spark
203                     We believe that the G37S knock-in mouse provides an excellent animal model for st
204 eckstrin homology (PH) domain point mutation knock-in mouse (R302, 303A), in which ARAP3 is uncoupled
205                                          The knock-in mouse represents an excellent mammalian model f
206          To address this question, we used a knock-in mouse, RMOR (for recycling MOR), in which genet
207 ion-dependent proteasomal degradation in the knock-in mouse RPE due to misfolding.
208 ing HDAC3 improves the phenotype of the SCA1 knock-in mouse (SCA1(154Q/2Q)), the most physiologically
209          Analysis of the Ter349Glu rhodopsin knock-in mouse showed a rapid, early onset degeneration
210 function in vivo in several tissues, using a knock-in mouse strain expressing a p53 mutant compromise
211                            An inbred genetic knock-in mouse strain expressing the variant BDNF recapi
212                      We recently described a knock-in mouse strain in which the substitution of 2 ami
213              In addition, the Runx1-IRES-GFP knock-in mouse strain should prove valuable for investig
214 oped a Flag- and hemagglutinin-tagged Fancd2 knock-in mouse strain that allowed a high throughput mas
215                                        A FMF-knock-in mouse strain that expresses chimeric pyrin prot
216 st this hypothesis, we used an Id2-CreER(T2) knock-in mouse strain to lineage trace the distal epithe
217 ar composition of these nAChRs, we studied a knock-in mouse strain with a leucine-to-alanine mutation
218 ed Flag- and haemagglutinin-tagged cyclin D1 knock-in mouse strains that allowed a high-throughput ma
219 models of HD, the R6/2 transgenic and CAG140 knock-in mouse strains, we demonstrate that adipose tiss
220 de, which predate overt pathology in Hdh CAG knock-in mouse striatum, implicate enhanced N-methyl-D-a
221                          For example, recent knock-in mouse studies have shown that MDM2 heterooligom
222                                 However, the knock-in mouse survives and develops a wide range of str
223 curate model of disease, we have generated a knock-in mouse (T32KI) carrying the c.1465G > A (p.D489N
224                               We developed a knock-in mouse that biologically recapitulates a common
225 lation in vivo, we used a Cys42Ser PKG1alpha knock-in mouse that cannot transduce oxidant signals bec
226 nt CK2 activation in T cells, we generated a knock-in mouse that expresses a CD5 protein containing a
227 e of NF-kappaB in inflammation, we created a knock-in mouse that expresses a constitutively active fo
228                                To do this, a knock-in mouse that expresses an RGS-insensitive (RGSi)
229 To address this issue, we generated a double knock-in mouse that expresses V regions of a somatically
230 nerated a floxed tandem dye (td)Tomato-C5aR2 knock-in mouse that we used to track C5aR2 expression in
231                                            A knock-in mouse was produced that replaced GFRalpha1 with
232                              This redox-dead knock-in mouse was substantively deficient in hypotensiv
233 d tandem-dye Tomato (tdTomato)-C3aR reporter knock-in mouse, which we used to monitor C3aR expression
234                                    The C5aR2 knock-in mouse will help to reliably track and condition
235                              The floxed C3aR knock-in mouse will help to reliably track and condition
236              The novel floxed C5aR1 reporter knock-in mouse will prove useful to track C5aR1 expressi
237 us in development and leukemia, we created a knock-in mouse with a C-terminal truncation by introduci
238                                      Using a knock-in mouse with a mutated ERalpha eliminating bindin
239 ycan in the aetiology of DMD, we generated a knock-in mouse with a phenylalanine substitution at a ke
240                       Herein, we generated a knock-in mouse with a targeted mutation in the immunorec
241  in IL-7-mediated B cell development using a knock-in mouse with a Tyr to Phe mutation (IL-7Ralpha(44
242       We have generated a novel MeCP2 mutant knock-in mouse with the mutation R168X, one of the most

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