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Jackson Laboratory lmnaflox/flox mutant mouse
Lmnaflox/Flox Mutant Mouse, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews

lmnaflox/flox mutant mouse - by Bioz Stars, 2026-04

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S232D mice do not demonstrate deficits in open field, grip strength, or rotor rod tests . (A) Quantification of distance traveled in the open field task at 3, 9, and 12 months. n =11-28 mice per group. Error bars represent s.e.m. (B) Quantification of grip strength at 3, 9, and 12 months. n =6-15 mice per group. Error bars represent s.e.m. (C) Quantification of latency to fall in rotor rod at 3, 9, and 12 months. n =11-28 mice per group. Error bars represent s.e.m. (D) Quantification of average latency to fall on the two test days at 3, 9, and 12 months. n =11-28 mice per group. Error bars represent s.e.m.

Journal: Biology Open

Article Title: A novel 14-3-3θ phosphomimetic mouse model demonstrates social dominance defects

doi: 10.1242/bio.061963

Figure Lengend Snippet: S232D mice do not demonstrate deficits in open field, grip strength, or rotor rod tests . (A) Quantification of distance traveled in the open field task at 3, 9, and 12 months. n =11-28 mice per group. Error bars represent s.e.m. (B) Quantification of grip strength at 3, 9, and 12 months. n =6-15 mice per group. Error bars represent s.e.m. (C) Quantification of latency to fall in rotor rod at 3, 9, and 12 months. n =11-28 mice per group. Error bars represent s.e.m. (D) Quantification of average latency to fall on the two test days at 3, 9, and 12 months. n =11-28 mice per group. Error bars represent s.e.m.

Article Snippet: As previously described, Cyagen created the conditional KI mouse expressing the 14-3-3θ S232D mutant ( ).

Techniques:

S232D mice are impaired in four-paw wire hang. (A) Quantification of latency to fall from wire hang apparatus at 3, 9, and 12 months. n =11-28 mice per group. * P ≤0.05 (unpaired, two-tailed t -test). Error bars represent s.e.m. (B) Mouse weights at 3, 9, and 12 months. n =11-28 mice per group. * P ≤0.05 (unpaired, two-tailed t -test). Error bars represent s.e.m. (C) Holding impulse, calculated as weight in grams multiplied by the hang time in seconds, at 3, 9, and 12 months. n =11-28 mice per group. * P ≤0.05 (unpaired, two-tailed t -test). Error bars represent s.e.m.

Journal: Biology Open

Article Title: A novel 14-3-3θ phosphomimetic mouse model demonstrates social dominance defects

doi: 10.1242/bio.061963

Figure Lengend Snippet: S232D mice are impaired in four-paw wire hang. (A) Quantification of latency to fall from wire hang apparatus at 3, 9, and 12 months. n =11-28 mice per group. * P ≤0.05 (unpaired, two-tailed t -test). Error bars represent s.e.m. (B) Mouse weights at 3, 9, and 12 months. n =11-28 mice per group. * P ≤0.05 (unpaired, two-tailed t -test). Error bars represent s.e.m. (C) Holding impulse, calculated as weight in grams multiplied by the hang time in seconds, at 3, 9, and 12 months. n =11-28 mice per group. * P ≤0.05 (unpaired, two-tailed t -test). Error bars represent s.e.m.

Article Snippet: As previously described, Cyagen created the conditional KI mouse expressing the 14-3-3θ S232D mutant ( ).

Techniques: Two Tailed Test

S232D mice show impairments in social dominance . (A) Quantification of tube test win rate of S232D mice matched against Cre control mice at 3 months of age. n =5-14 mice per group. *** P ≤0.001 (unpaired, two-tailed t -test). Error bars represent s.e.m. (B) Quantification of tube test win rate of WT control mice matched against Cre control mice at 3 months of age. n =5-12 mice per group. Error bars represent s.e.m. (C) Quantification of tube test win rate of S232D mice matched against WT control mice at 3 months of age. n =10-13 mice per group. P =0.054 (unpaired, two-tailed t -test). Error bars represent s.e.m. (D) Quantification of tube test win rate of S232D mice matched against WT control mice at 9 months of age. n =10-13 mice per group. *** P ≤0.001 (unpaired, two-tailed t -test). Error bars represent s.e.m. (E) Quantification of tube test win rate of S232D mice matched against WT control mice at 12 months of age. n =10-12 mice per group. **** P ≤0.0001 (unpaired, two-tailed t -test). Error bars represent s.e.m.

Journal: Biology Open

Article Title: A novel 14-3-3θ phosphomimetic mouse model demonstrates social dominance defects

doi: 10.1242/bio.061963

Figure Lengend Snippet: S232D mice show impairments in social dominance . (A) Quantification of tube test win rate of S232D mice matched against Cre control mice at 3 months of age. n =5-14 mice per group. *** P ≤0.001 (unpaired, two-tailed t -test). Error bars represent s.e.m. (B) Quantification of tube test win rate of WT control mice matched against Cre control mice at 3 months of age. n =5-12 mice per group. Error bars represent s.e.m. (C) Quantification of tube test win rate of S232D mice matched against WT control mice at 3 months of age. n =10-13 mice per group. P =0.054 (unpaired, two-tailed t -test). Error bars represent s.e.m. (D) Quantification of tube test win rate of S232D mice matched against WT control mice at 9 months of age. n =10-13 mice per group. *** P ≤0.001 (unpaired, two-tailed t -test). Error bars represent s.e.m. (E) Quantification of tube test win rate of S232D mice matched against WT control mice at 12 months of age. n =10-12 mice per group. **** P ≤0.0001 (unpaired, two-tailed t -test). Error bars represent s.e.m.

Article Snippet: As previously described, Cyagen created the conditional KI mouse expressing the 14-3-3θ S232D mutant ( ).

Techniques: Control, Two Tailed Test

S232D mice do not display anxiety or cognitive deficits. (A) Quantification of time spent in the open arm in the elevated plus maze (EPM) or elevated zero maze (EZM) at 3, 9, and 12 months. n =5-13 mice per group. Error bars represent s.e.m. (B) Quantification of latency in crossing to the dark side on day 2 of the passive avoidance task at 12 months. n =11-25 mice per group. Error bars represent s.e.m. (C) Quantification of latency to platform in the Morris water maze (MWM) at 3, 9, and 12 months. n =5-13 mice per group. * P ≤0.05 (two-way repeated ANOVA). Error bars represent s.e.m. (D) Quantification of the probe trial in the MWM at 3, 9, and 12 months. n =5-13 mice per group. Error bars represent s.e.m.

Journal: Biology Open

Article Title: A novel 14-3-3θ phosphomimetic mouse model demonstrates social dominance defects

doi: 10.1242/bio.061963

Figure Lengend Snippet: S232D mice do not display anxiety or cognitive deficits. (A) Quantification of time spent in the open arm in the elevated plus maze (EPM) or elevated zero maze (EZM) at 3, 9, and 12 months. n =5-13 mice per group. Error bars represent s.e.m. (B) Quantification of latency in crossing to the dark side on day 2 of the passive avoidance task at 12 months. n =11-25 mice per group. Error bars represent s.e.m. (C) Quantification of latency to platform in the Morris water maze (MWM) at 3, 9, and 12 months. n =5-13 mice per group. * P ≤0.05 (two-way repeated ANOVA). Error bars represent s.e.m. (D) Quantification of the probe trial in the MWM at 3, 9, and 12 months. n =5-13 mice per group. Error bars represent s.e.m.

Article Snippet: As previously described, Cyagen created the conditional KI mouse expressing the 14-3-3θ S232D mutant ( ).

Techniques:

$αSyn and phospho-tau levels are not altered in S232D mice. (A) Representative images and quantification of αsyn immunostaining of S232D and WT control cortical tissue with and without digestion with proteinase K (PK). n =10-12 mice per group. Error bars represent s.e.m. (B) Quantification of mRNA levels of 14-3-3θ normalized to actin in the cortices of 12 month old S232D and Cre control mice. n =4 mice per group. Error bars represent s.e.m. (C) Representative Western blot and quantification of αsyn and 14-3-3θ levels in Triton X-100 soluble cortical fractions from 3-month-old S232D, Cre control, and WT control brains. n =3 mice per group. Error bars represent s.e.m. (D) Representative Western blot and quantification of αsyn and 14-3-3θ levels in Triton X-100 insoluble cortical fractions from 3-month-old S232D, Cre control, and WT control brains. n =3 mice per group. Error bars represent s.e.m. (E) Representative Western blot and quantification of αsyn, 14-3-3θ, and ptau levels in Triton X-100 soluble cortical fractions from 12-month-old S232D and Cre control brains. n =4 mice per group. * P ≤0.05 (unpaired, two-tailed t -test). Error bars represent s.e.m. (F) Representative Western blot and quantification of αsyn, 14-3-3θ, and ptau levels in Triton X-100 insoluble cortical fractions from 12-month-old S232D and Cre control brains. n =4 mice per group. * P ≤0.05 (unpaired, two-tailed t -test). Error bars represent s.e.m.$

Journal: Biology Open

Article Title: A novel 14-3-3θ phosphomimetic mouse model demonstrates social dominance defects

doi: 10.1242/bio.061963

Figure Lengend Snippet: αSyn and phospho-tau levels are not altered in S232D mice. (A) Representative images and quantification of αsyn immunostaining of S232D and WT control cortical tissue with and without digestion with proteinase K (PK). n =10-12 mice per group. Error bars represent s.e.m. (B) Quantification of mRNA levels of 14-3-3θ normalized to actin in the cortices of 12 month old S232D and Cre control mice. n =4 mice per group. Error bars represent s.e.m. (C) Representative Western blot and quantification of αsyn and 14-3-3θ levels in Triton X-100 soluble cortical fractions from 3-month-old S232D, Cre control, and WT control brains. n =3 mice per group. Error bars represent s.e.m. (D) Representative Western blot and quantification of αsyn and 14-3-3θ levels in Triton X-100 insoluble cortical fractions from 3-month-old S232D, Cre control, and WT control brains. n =3 mice per group. Error bars represent s.e.m. (E) Representative Western blot and quantification of αsyn, 14-3-3θ, and ptau levels in Triton X-100 soluble cortical fractions from 12-month-old S232D and Cre control brains. n =4 mice per group. * P ≤0.05 (unpaired, two-tailed t -test). Error bars represent s.e.m. (F) Representative Western blot and quantification of αsyn, 14-3-3θ, and ptau levels in Triton X-100 insoluble cortical fractions from 12-month-old S232D and Cre control brains. n =4 mice per group. * P ≤0.05 (unpaired, two-tailed t -test). Error bars represent s.e.m.

Article Snippet: As previously described, Cyagen created the conditional KI mouse expressing the 14-3-3θ S232D mutant ( ).

Techniques: Immunostaining, Control, Western Blot, Two Tailed Test

Dendritic architecture is unchanged in neurons from S232D mice. (A) Representative images of MAP2 immunostaining of S232D and Cre control primary neurons at DIV 8. (B) Quantification of neurite length of S232D and Cre control primary neurons at DIV 8. n =3 independent rounds with 10-12 neurons per group per round. Error bars represent s.e.m. (C) Quantification of number of primary dendrites of S232D and Cre control primary neurons at DIV 8. n =3 independent rounds with 10-12 neurons per group per round. Error bars represent s.e.m. (D) Quantification of number of nodes of S232D and Cre control primary neurons at DIV 8. n =3 independent rounds with 10-12 neurons per group per round. Error bars represent s.e.m. (E) Quantification of number of terminal ends of S232D and Cre control primary neurons at DIV 8. n =3 independent rounds with 10-12 neurons per group per round. Error bars represent s.e.m. (F) Scholl analysis of S232D and Cre control primary neurons at DIV 8. n =3 independent rounds with 10-12 neurons per group per round. (G) Quantification of the area under the curve in the Scholl analysis of S232D and Cre primary neurons. n =3 independent rounds with 10-12 neurons per group per round. Error bars represent s.e.m.

Journal: Biology Open

Article Title: A novel 14-3-3θ phosphomimetic mouse model demonstrates social dominance defects

doi: 10.1242/bio.061963

Figure Lengend Snippet: Dendritic architecture is unchanged in neurons from S232D mice. (A) Representative images of MAP2 immunostaining of S232D and Cre control primary neurons at DIV 8. (B) Quantification of neurite length of S232D and Cre control primary neurons at DIV 8. n =3 independent rounds with 10-12 neurons per group per round. Error bars represent s.e.m. (C) Quantification of number of primary dendrites of S232D and Cre control primary neurons at DIV 8. n =3 independent rounds with 10-12 neurons per group per round. Error bars represent s.e.m. (D) Quantification of number of nodes of S232D and Cre control primary neurons at DIV 8. n =3 independent rounds with 10-12 neurons per group per round. Error bars represent s.e.m. (E) Quantification of number of terminal ends of S232D and Cre control primary neurons at DIV 8. n =3 independent rounds with 10-12 neurons per group per round. Error bars represent s.e.m. (F) Scholl analysis of S232D and Cre control primary neurons at DIV 8. n =3 independent rounds with 10-12 neurons per group per round. (G) Quantification of the area under the curve in the Scholl analysis of S232D and Cre primary neurons. n =3 independent rounds with 10-12 neurons per group per round. Error bars represent s.e.m.

Article Snippet: As previously described, Cyagen created the conditional KI mouse expressing the 14-3-3θ S232D mutant ( ).

Techniques: Immunostaining, Control

$NMDA receptor levels in the cortex . (A) Representative Western blot of NMDAR1, NMDAR2A, NMDAR2B, PSD95, and total protein in post-synaptic density (PSD) fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. (B) Quantification of NMDAR1 normalized to PSD95 in PSD fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. Error bars represent s.e.m. (C) Quantification of NMDAR2A normalized to PSD95 in PSD fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. *** P ≤0.001 (unpaired, two-tailed t -test). Error bars represent s.e.m. (D) Quantification of NMDAR2B normalized to PSD95 in PSD fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. *** P ≤0.001 (unpaired, two-tailed t -test). Error bars represent s.e.m. (E) Quantification of PSD95 normalized to total protein in PSD fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. Error bars represent s.e.m. (F) Quantification of NMDAR1 normalized to total protein in PSD fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. Error bars represent s.e.m. (G) Quantification of NMDAR2A normalized to total protein in PSD fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. Error bars represent s.e.m. (H) Quantification of NMDAR2B normalized to total protein in PSD fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. Error bars represent s.e.m.$

Journal: Biology Open

Article Title: A novel 14-3-3θ phosphomimetic mouse model demonstrates social dominance defects

doi: 10.1242/bio.061963

Figure Lengend Snippet: NMDA receptor levels in the cortex . (A) Representative Western blot of NMDAR1, NMDAR2A, NMDAR2B, PSD95, and total protein in post-synaptic density (PSD) fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. (B) Quantification of NMDAR1 normalized to PSD95 in PSD fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. Error bars represent s.e.m. (C) Quantification of NMDAR2A normalized to PSD95 in PSD fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. *** P ≤0.001 (unpaired, two-tailed t -test). Error bars represent s.e.m. (D) Quantification of NMDAR2B normalized to PSD95 in PSD fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. *** P ≤0.001 (unpaired, two-tailed t -test). Error bars represent s.e.m. (E) Quantification of PSD95 normalized to total protein in PSD fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. Error bars represent s.e.m. (F) Quantification of NMDAR1 normalized to total protein in PSD fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. Error bars represent s.e.m. (G) Quantification of NMDAR2A normalized to total protein in PSD fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. Error bars represent s.e.m. (H) Quantification of NMDAR2B normalized to total protein in PSD fractions from the cortices of 3-month-old S232D and Cre control brains. n =6 mice per group. Error bars represent s.e.m.

Article Snippet: As previously described, Cyagen created the conditional KI mouse expressing the 14-3-3θ S232D mutant ( ).

Techniques: Western Blot, Control, Two Tailed Test

Altered skeletal development in Col4a1 + /Δex41 mice. (A) Col4a1 + /Δex41 mice exhibit reduced body size compared to their Col4a1 +/+ littermates throughout life (shown are postnatal day (P) 7 mice). (B-H) Representative images of skeletal preparations from P7 mice stained with Alcian blue and Alizarin red showing reduced ossification in (C-D) calvaria (black arrow indicate reduced Alizarin red staining), (E-F) ribs (black asterisks demarcate regions where alizarin red staining is absent in E and F), and (E-H) vertebrae (white asterisks mark the vertebral column in E and F) from Col4a1 + /Δex41 mice compared to sex-matched Col4a1 +/+ littermates. n = 3 mice per genotype. Shown are skeletal preparations from male mice, similar results were observed in female mice.

Journal: Matrix biology : journal of the International Society for Matrix Biology

Article Title: Skeletal pathology in mouse models of Gould syndrome is partially alleviated by genetically reducing TGFβ signaling

doi: 10.1016/j.matbio.2024.07.005

Figure Lengend Snippet: Altered skeletal development in Col4a1 + /Δex41 mice. (A) Col4a1 + /Δex41 mice exhibit reduced body size compared to their Col4a1 +/+ littermates throughout life (shown are postnatal day (P) 7 mice). (B-H) Representative images of skeletal preparations from P7 mice stained with Alcian blue and Alizarin red showing reduced ossification in (C-D) calvaria (black arrow indicate reduced Alizarin red staining), (E-F) ribs (black asterisks demarcate regions where alizarin red staining is absent in E and F), and (E-H) vertebrae (white asterisks mark the vertebral column in E and F) from Col4a1 + /Δex41 mice compared to sex-matched Col4a1 +/+ littermates. n = 3 mice per genotype. Shown are skeletal preparations from male mice, similar results were observed in female mice.

Article Snippet: The conditional Col4a1 Flex41 mutant mouse was generated by InGenious Targeting Laboratory (Stony Brook, NY) and previously characterized and validated [ , ].

Techniques: Staining

Altered bone marker gene expression in P7 Col4a1 + /Δex41 mice. (A-B) qPCR analyses showing altered expression of bone marker genes in calvaria (A) and femurs (B) from P7 Col4a1 + /Δex41 mice compared to their Col4a1 +/+ littermates. Expression of bone marker genes was normalized to the expression of β2-microglobulin . Data are presented as fold expression relative to Col4a1 +/+ levels, mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001, unpaired two-tailed Student t -test. Since no difference in bone marker gene expression were observed between male and female mice, both sexes were combined with similar numbers of males and females included.

Journal: Matrix biology : journal of the International Society for Matrix Biology

Article Title: Skeletal pathology in mouse models of Gould syndrome is partially alleviated by genetically reducing TGFβ signaling

doi: 10.1016/j.matbio.2024.07.005

Figure Lengend Snippet: Altered bone marker gene expression in P7 Col4a1 + /Δex41 mice. (A-B) qPCR analyses showing altered expression of bone marker genes in calvaria (A) and femurs (B) from P7 Col4a1 + /Δex41 mice compared to their Col4a1 +/+ littermates. Expression of bone marker genes was normalized to the expression of β2-microglobulin . Data are presented as fold expression relative to Col4a1 +/+ levels, mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001, unpaired two-tailed Student t -test. Since no difference in bone marker gene expression were observed between male and female mice, both sexes were combined with similar numbers of males and females included.

Article Snippet: The conditional Col4a1 Flex41 mutant mouse was generated by InGenious Targeting Laboratory (Stony Brook, NY) and previously characterized and validated [ , ].

Techniques: Marker, Gene Expression, Expressing, Two Tailed Test

$Morphometric analyses of femoral cortical and trabecular bone in Col4a1 + /Δex41 mice. (A-B) Representative 3D images generated from microcomputed tomography (μCT) analysis of cortical and trabecular parameters of femurs from 3 to 4 months old female (A) and male (B) Col4a1 +/+ and Col4a1 + /Δex41 mice. Scale bar=200μm. (C-J) Bone parameters of femurs analyzed by μCT. (C-E) Cortical bone parameters of the middle diaphysis. While cortical bone area fraction (Ct.Ar/T.Ar) (C) and cortical bone mineral density (BMD) (E) were not significantly different between genotypes, cortical bone thickness was significantly reduced in Col4a1 + /Δex41 mice compared to sex-matched Col4a1 +/+ littermates (D). (F-J) Femoral trabecular bone parameters. Trabecular bone volume fraction (BV/TV) (F) and trabecular number (G) were significantly reduced and spacing (H) was significantly increased both in female and male Col4a1 + /Δex41 mice compared to sex-matched Col4a1 +/+ littermates, while trabecular thickness was significantly reduced in male, but not female Col4a1 + /Δex41 mice (I). Trabecular BMD was also reduced in Col4a1 + /Δex41 mice compared to their sex-matched Col4a1 +/+ littermates (J). n = 8 for Col4a1 +/+ and Col4a1 + /Δex41 female mice and n = 9 and 7 for Col4a1 +/+ and Col4a1 + /Δex41 male mice, respectively. Data are presented as mean ± SD. * p ≤ 0.05, ** p < 0.01, *** p < 0.001, unpaired two-tailed Student t -test. Additional parameters are shown in .$

Journal: Matrix biology : journal of the International Society for Matrix Biology

Article Title: Skeletal pathology in mouse models of Gould syndrome is partially alleviated by genetically reducing TGFβ signaling

doi: 10.1016/j.matbio.2024.07.005

Figure Lengend Snippet: Morphometric analyses of femoral cortical and trabecular bone in Col4a1 + /Δex41 mice. (A-B) Representative 3D images generated from microcomputed tomography (μCT) analysis of cortical and trabecular parameters of femurs from 3 to 4 months old female (A) and male (B) Col4a1 +/+ and Col4a1 + /Δex41 mice. Scale bar=200μm. (C-J) Bone parameters of femurs analyzed by μCT. (C-E) Cortical bone parameters of the middle diaphysis. While cortical bone area fraction (Ct.Ar/T.Ar) (C) and cortical bone mineral density (BMD) (E) were not significantly different between genotypes, cortical bone thickness was significantly reduced in Col4a1 + /Δex41 mice compared to sex-matched Col4a1 +/+ littermates (D). (F-J) Femoral trabecular bone parameters. Trabecular bone volume fraction (BV/TV) (F) and trabecular number (G) were significantly reduced and spacing (H) was significantly increased both in female and male Col4a1 + /Δex41 mice compared to sex-matched Col4a1 +/+ littermates, while trabecular thickness was significantly reduced in male, but not female Col4a1 + /Δex41 mice (I). Trabecular BMD was also reduced in Col4a1 + /Δex41 mice compared to their sex-matched Col4a1 +/+ littermates (J). n = 8 for Col4a1 +/+ and Col4a1 + /Δex41 female mice and n = 9 and 7 for Col4a1 +/+ and Col4a1 + /Δex41 male mice, respectively. Data are presented as mean ± SD. * p ≤ 0.05, ** p < 0.01, *** p < 0.001, unpaired two-tailed Student t -test. Additional parameters are shown in .

Article Snippet: The conditional Col4a1 Flex41 mutant mouse was generated by InGenious Targeting Laboratory (Stony Brook, NY) and previously characterized and validated [ , ].

Techniques: Generated, Tomography, Two Tailed Test

Altered bone mechanical properties in Col4a1 + /Δex41 mice. (A-D) Assessment of femoral bone mechanical properties by 3-point bending flexural test revealed a trend toward reduced femoral stiffness in Col4a1 + /Δex41 mice compared to sex-matched Col4a1 +/+ littermates (A), a significant reduction in yield force in female but not male Col4a1 + /Δex41 mice (B), a decrease in ultimate force that reached statistical significance in male but not female Col4a1 + /Δex41 mice (C), and a significant decrease in work in male but not female Col4a1 + /Δex41 mice (D). n = 4/group. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01, unpaired two-tailed Student t -test. Additional details are shown in .

Journal: Matrix biology : journal of the International Society for Matrix Biology

Article Title: Skeletal pathology in mouse models of Gould syndrome is partially alleviated by genetically reducing TGFβ signaling

doi: 10.1016/j.matbio.2024.07.005

Figure Lengend Snippet: Altered bone mechanical properties in Col4a1 + /Δex41 mice. (A-D) Assessment of femoral bone mechanical properties by 3-point bending flexural test revealed a trend toward reduced femoral stiffness in Col4a1 + /Δex41 mice compared to sex-matched Col4a1 +/+ littermates (A), a significant reduction in yield force in female but not male Col4a1 + /Δex41 mice (B), a decrease in ultimate force that reached statistical significance in male but not female Col4a1 + /Δex41 mice (C), and a significant decrease in work in male but not female Col4a1 + /Δex41 mice (D). n = 4/group. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01, unpaired two-tailed Student t -test. Additional details are shown in .

Article Snippet: The conditional Col4a1 Flex41 mutant mouse was generated by InGenious Targeting Laboratory (Stony Brook, NY) and previously characterized and validated [ , ].

Techniques: Two Tailed Test

$Morphometric analyses of femoral cortical and trabecular bones in Col4a1 + /G394V and Col4a1 + /G1344D mice. (A-B) Representative 3D images generated from μCT analysis of cortical and trabecular bone parameter of femurs from 3 to 4mo (A) female and (B) male Col4a1 +/+ , Col4a1 + /G394V , and Col4a1 + /G1344D mice. Scale bar=200μm. (C-J) Bone parameters of femurs analyzed by μCT. (C-E) Cortical bone parameters of the middle diaphysis, including cortical bone area fraction (Ct.Ar/T.Ar) (C), cortical bone thickness (D) and cortical BMD (E), were similar between Col4a1 + /mut mice and their Col4a1 +/+ littermates. (F-J) Femoral trabecular bone parameters. Trabecular bone density (BV/TV) (F) and trabecular numbers (G) are reduced, and trabecular separation (H) increased in Col4a1 + /mut mice compared to Col4a1 +/+ littermates. Femoral trabecular thickness (I) was slightly increased in Col4a1 + /G394V females compared to sex-matched Col4a1 +/+ and Col4a1 + /G1344D mice and a trend towards reduced BMD was observed in Col4a1 + /G394V mice compared to Col4a1 +/+ mice (J). n = 11, 5, and 10 for Col4a1 +/+ , Col4a1 + /G394V , and Col4a1 + /G1344D female mice, and n = 11, 6, and 8 for Col4a1 +/+ , Col4a1 + /G394V , and Col4a1 + /G1344D male mice, respectively. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001, one-way ANOVA. Additional parameters are shown in .$

Journal: Matrix biology : journal of the International Society for Matrix Biology

Article Title: Skeletal pathology in mouse models of Gould syndrome is partially alleviated by genetically reducing TGFβ signaling

doi: 10.1016/j.matbio.2024.07.005

Figure Lengend Snippet: Morphometric analyses of femoral cortical and trabecular bones in Col4a1 + /G394V and Col4a1 + /G1344D mice. (A-B) Representative 3D images generated from μCT analysis of cortical and trabecular bone parameter of femurs from 3 to 4mo (A) female and (B) male Col4a1 +/+ , Col4a1 + /G394V , and Col4a1 + /G1344D mice. Scale bar=200μm. (C-J) Bone parameters of femurs analyzed by μCT. (C-E) Cortical bone parameters of the middle diaphysis, including cortical bone area fraction (Ct.Ar/T.Ar) (C), cortical bone thickness (D) and cortical BMD (E), were similar between Col4a1 + /mut mice and their Col4a1 +/+ littermates. (F-J) Femoral trabecular bone parameters. Trabecular bone density (BV/TV) (F) and trabecular numbers (G) are reduced, and trabecular separation (H) increased in Col4a1 + /mut mice compared to Col4a1 +/+ littermates. Femoral trabecular thickness (I) was slightly increased in Col4a1 + /G394V females compared to sex-matched Col4a1 +/+ and Col4a1 + /G1344D mice and a trend towards reduced BMD was observed in Col4a1 + /G394V mice compared to Col4a1 +/+ mice (J). n = 11, 5, and 10 for Col4a1 +/+ , Col4a1 + /G394V , and Col4a1 + /G1344D female mice, and n = 11, 6, and 8 for Col4a1 +/+ , Col4a1 + /G394V , and Col4a1 + /G1344D male mice, respectively. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001, one-way ANOVA. Additional parameters are shown in .

Article Snippet: The conditional Col4a1 Flex41 mutant mouse was generated by InGenious Targeting Laboratory (Stony Brook, NY) and previously characterized and validated [ , ].

Techniques: Generated

$Genetically reducing Tgfb1 levels partially improves structural bone parameters in Col4a1 + /Δex41 mice. Morphometric analyses of femurs from 3 to 4 mo male mice. (A-B) Representative 3D images generated from μCT analysis of cortical and trabecular femoral bones from 3 to 4mo untreated (NT), 4PBA-treated, and Tgfb1 heterozygous Col4a1 +/+ (A) and Col4a1 + /Δex41 (B) mice. Scale bar=200μm. (C-E) Cortical bone parameters of the middle diaphysis and (F-J) trabecular bone parameters analyzed by μCT showing significant reductions in cortical thickness, trabecular bone density and number and significant increase in trabecular separation in untreated Col4a1 + /Δex41 mice compared their Col4a1 +/+ counterparts (D, F, G, and H, respectively). 4PBA treatment increased trabecular bone volume fraction and cortical and trabecular thicknesses in Col4a1 +/+ mice (F, D, and I). Although 4PBA improved trabecular number and separation (G, H) in Col4a1 + /Δex41 mice, it significantly decreased trabecular bone thickness and BMD (I and J). While Tgfb1 heterozygosity significantly reduced cortical and trabecular thickness and tended to reduce cortical BMD and trabecular bone volume fraction in Col4a1 +/+ mice (D, I, E, and F), it significantly improved trabecular bone number and separation and tended to increase trabecular bone volume fraction in Col4a1 + /Δex41 mice (G, H, and F, respectively). n = 9, 10, 8 for untreated, 4PBA-treated and Tgfb1 +/− Col4a1 +/+ mice and n = 12, 8, and 7 for untreated, 4PBA-treated and Tgfb1 +/− Col4a1 + /Δex41 mice, respectively. Data are presented as mean ± SD. ** P < 0.01; **** P < 0.0001, unpaired two-tailed Student t -test for comparison between untreated Col4a1 +/+ and Col4a1 + /Δex41 mice. ‡ p < 0.05; ‡‡ p < 0.001, one-way ANOVA (or Kruskal-Wallis and Dunnett pairwise tests for non-Gaussian distribution in F and H) to test the effect of 4PBA treatment and Tgfb1 heterozygosity in mice of a given genotype. Additional parameters are shown in .$

Journal: Matrix biology : journal of the International Society for Matrix Biology

Article Title: Skeletal pathology in mouse models of Gould syndrome is partially alleviated by genetically reducing TGFβ signaling

doi: 10.1016/j.matbio.2024.07.005

Figure Lengend Snippet: Genetically reducing Tgfb1 levels partially improves structural bone parameters in Col4a1 + /Δex41 mice. Morphometric analyses of femurs from 3 to 4 mo male mice. (A-B) Representative 3D images generated from μCT analysis of cortical and trabecular femoral bones from 3 to 4mo untreated (NT), 4PBA-treated, and Tgfb1 heterozygous Col4a1 +/+ (A) and Col4a1 + /Δex41 (B) mice. Scale bar=200μm. (C-E) Cortical bone parameters of the middle diaphysis and (F-J) trabecular bone parameters analyzed by μCT showing significant reductions in cortical thickness, trabecular bone density and number and significant increase in trabecular separation in untreated Col4a1 + /Δex41 mice compared their Col4a1 +/+ counterparts (D, F, G, and H, respectively). 4PBA treatment increased trabecular bone volume fraction and cortical and trabecular thicknesses in Col4a1 +/+ mice (F, D, and I). Although 4PBA improved trabecular number and separation (G, H) in Col4a1 + /Δex41 mice, it significantly decreased trabecular bone thickness and BMD (I and J). While Tgfb1 heterozygosity significantly reduced cortical and trabecular thickness and tended to reduce cortical BMD and trabecular bone volume fraction in Col4a1 +/+ mice (D, I, E, and F), it significantly improved trabecular bone number and separation and tended to increase trabecular bone volume fraction in Col4a1 + /Δex41 mice (G, H, and F, respectively). n = 9, 10, 8 for untreated, 4PBA-treated and Tgfb1 +/− Col4a1 +/+ mice and n = 12, 8, and 7 for untreated, 4PBA-treated and Tgfb1 +/− Col4a1 + /Δex41 mice, respectively. Data are presented as mean ± SD. ** P < 0.01; **** P < 0.0001, unpaired two-tailed Student t -test for comparison between untreated Col4a1 +/+ and Col4a1 + /Δex41 mice. ‡ p < 0.05; ‡‡ p < 0.001, one-way ANOVA (or Kruskal-Wallis and Dunnett pairwise tests for non-Gaussian distribution in F and H) to test the effect of 4PBA treatment and Tgfb1 heterozygosity in mice of a given genotype. Additional parameters are shown in .

Article Snippet: The conditional Col4a1 Flex41 mutant mouse was generated by InGenious Targeting Laboratory (Stony Brook, NY) and previously characterized and validated [ , ].

Techniques: Generated, Two Tailed Test, Comparison

4PBA and Tgfb1 heterozygosity do not ameliorate alterations in bone mechanical and material properties in Col4a1 + /Δex41 mice. (A-F) 3-point bending flexural analysis of femurs from 3 to 4mo male mice showing altered femoral bone mechanical (A-C) and material (D-F) properties characterized by significant reductions in stiffness (A) and maximal load (C) and significant increase in elastic modulus (D) in Col4a1 + /Δex41 mice compared to Col4a1 +/+ mice. Neither 4PBA treatment nor Tgfb1 heterozygosity improved bone mechanical and material properties in Col4a1 + /Δex41 mice. 4PBA treatment did not affect bone mechanical and material properties in Col4a1 +/+ mice (A-F) but it exacerbated the reduction in femoral stiffness in Col4a1 + /Δex41 mice (A). While Tgfb1 heterozygosity had deleterious effects in Col4a1 +/+ mice, including significant reduction in maximal load (C) and increase in elastic modulus (D), it did not affect mechanical and material bone parameters in Col4a1 + /Δex41 mice. n = 9, 10, 8 for untreated, 4PBA-treated and Tgfb1 +/− Col4a1 +/+ mice, and n = 12, 8, and 7 for untreated, 4PBA-treated and Tgfb1 +/− Col4a1 + /Δex41 mice, respectively. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; **** p < 0.0001, unpaired two-tailed Student t -test for comparison between untreated Col4a1 +/+ and Col4a1 + /Δex41 mice. ‡ p < 0.05; ‡‡ p < 0.001, one-way ANOVA (or Kruskal-Wallis and Dunnett pairwise tests for non-Gaussian distribution in A and F) to test the effect of 4PBA treatment and Tgfb1 heterozygosity in mice of a given genotype. Additional details are shown in .

Journal: Matrix biology : journal of the International Society for Matrix Biology

Article Title: Skeletal pathology in mouse models of Gould syndrome is partially alleviated by genetically reducing TGFβ signaling

doi: 10.1016/j.matbio.2024.07.005

Figure Lengend Snippet: 4PBA and Tgfb1 heterozygosity do not ameliorate alterations in bone mechanical and material properties in Col4a1 + /Δex41 mice. (A-F) 3-point bending flexural analysis of femurs from 3 to 4mo male mice showing altered femoral bone mechanical (A-C) and material (D-F) properties characterized by significant reductions in stiffness (A) and maximal load (C) and significant increase in elastic modulus (D) in Col4a1 + /Δex41 mice compared to Col4a1 +/+ mice. Neither 4PBA treatment nor Tgfb1 heterozygosity improved bone mechanical and material properties in Col4a1 + /Δex41 mice. 4PBA treatment did not affect bone mechanical and material properties in Col4a1 +/+ mice (A-F) but it exacerbated the reduction in femoral stiffness in Col4a1 + /Δex41 mice (A). While Tgfb1 heterozygosity had deleterious effects in Col4a1 +/+ mice, including significant reduction in maximal load (C) and increase in elastic modulus (D), it did not affect mechanical and material bone parameters in Col4a1 + /Δex41 mice. n = 9, 10, 8 for untreated, 4PBA-treated and Tgfb1 +/− Col4a1 +/+ mice, and n = 12, 8, and 7 for untreated, 4PBA-treated and Tgfb1 +/− Col4a1 + /Δex41 mice, respectively. Data are presented as mean ± SD. * p < 0.05; ** p < 0.01; **** p < 0.0001, unpaired two-tailed Student t -test for comparison between untreated Col4a1 +/+ and Col4a1 + /Δex41 mice. ‡ p < 0.05; ‡‡ p < 0.001, one-way ANOVA (or Kruskal-Wallis and Dunnett pairwise tests for non-Gaussian distribution in A and F) to test the effect of 4PBA treatment and Tgfb1 heterozygosity in mice of a given genotype. Additional details are shown in .

Article Snippet: The conditional Col4a1 Flex41 mutant mouse was generated by InGenious Targeting Laboratory (Stony Brook, NY) and previously characterized and validated [ , ].

Techniques: Two Tailed Test, Comparison

Reduced vascular density in femora from Col4a1 + /Δex41 mice. (A-B) Representative images and (C-E) quantification of synchrotron radiation micro-computed tomography (SRμCT) analysis of femoral longitudinal canals from 3 to 4 months old Col4a1 +/+ and Col4a1 + /Δex41 male mice. While vascular canal diameter was similar between Col4a1 +/+ and Col4a1 + /Δex41 mice (C), vascular canal density was significantly reduced in Col4a1 + /Δex41 mice (D) which was reflected in a trend towards decrease cortical porosity (E). Data are presented as mean ± SD. * p < 0.05.

Journal: Matrix biology : journal of the International Society for Matrix Biology

Article Title: Skeletal pathology in mouse models of Gould syndrome is partially alleviated by genetically reducing TGFβ signaling

doi: 10.1016/j.matbio.2024.07.005

Figure Lengend Snippet: Reduced vascular density in femora from Col4a1 + /Δex41 mice. (A-B) Representative images and (C-E) quantification of synchrotron radiation micro-computed tomography (SRμCT) analysis of femoral longitudinal canals from 3 to 4 months old Col4a1 +/+ and Col4a1 + /Δex41 male mice. While vascular canal diameter was similar between Col4a1 +/+ and Col4a1 + /Δex41 mice (C), vascular canal density was significantly reduced in Col4a1 + /Δex41 mice (D) which was reflected in a trend towards decrease cortical porosity (E). Data are presented as mean ± SD. * p < 0.05.

Article Snippet: The conditional Col4a1 Flex41 mutant mouse was generated by InGenious Targeting Laboratory (Stony Brook, NY) and previously characterized and validated [ , ].

Techniques: Micro-CT

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