Journal: Journal of Neuroinflammation

Article Title: Selective vulnerability of the aging cholinergic system to amyloid pathology revealed by induced APP overexpression

doi: 10.1186/s12974-025-03682-2

Figure Lengend Snippet: Autophagic activity in the mouse brain was modulated by both aging and mutant APP transgene expression. a Representative western blot images are shown. Autophagy-related targets assessed include ( b ) LC3A-II/LC3A-I ratio, ( c ) total LC3A, ( d ) LC3B-II/LC3B-I ratio, ( e ) total LC3B, ( f ) ATG3, ( g ) ATG5, ( h ) ATG7, ( i ) ATG12, ( j ) Beclin-1, and ( k ) SQSTM1/p62. Sample size was 5 male and 5 female 18mo controls, 4–5 male and 6 female APP 6 → 18mo, 4–5 male and 5 female 24mo controls, and 5 male and 5–6 female APP 12 → 24mo. Individual data points and group means ± S.E.M. are presented. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: Male mice overexpressing the tetO-APPswe/ind transgene (B6.Cg-Tg(tetO-APPSweInd)102Dbo/Mmjax; stock no. 34845-JAX; Jackson Laboratory, Bar Harbor, MA, USA) on a C57BL/6 background were obtained from Jackson Laboratory.

Techniques: Activity Assay, Mutagenesis, Expressing, Western Blot

Journal: Neural Regeneration Research

Article Title: FUBP3 mediates the amyloid-β-induced neuronal NLRP3 expression

doi: 10.4103/NRR.NRR-D-23-01799

Figure Lengend Snippet: NLRP3 is expressed in neurons and regulates tau phosphorylation. (A) Brain sections from 3-month-old wild-type mice were costained with antibodies to NLRP3 (red, Alexa Fluor 564) and the microglial marker Iba1 (green, Alexa Fluor 488). (B) Brain sections from 8-month-old APP/PS1ΔE9 AD model mice were costained with anti-NLRP3 (red, Alexa Fluor 564) and anti-Iba1 (green, Alexa Fluor 488) antibodies. Arrowheads indicate NLRP3-positive microglia, and the neuritic plaque is circled. (C) Brain sections from 8-month-old APP/PS1ΔE9 AD model mice were costained with anti-NLRP3 (red, Alexa Fluor 564) and anti-NeuN (green, Alexa Fluor 488) antibodies. The arrowhead indicates an NLRP3-positive neuron. (D) Hydrogen peroxide (H 2 O 2 ) was injected into the hippocampus of APP/PS1ΔE9 mice, and brain sections from these mice were costained with antibodies to NLRP3 and the neuronal marker NeuN. Arrowheads indicate NeuN-positive, NLRP3-negative neurons in the peri-injection area. The dashed boxes indicate the areas that are enlarged in the lower panels. (E) Western blot analysis of lysates from the microglial cell line BV2 and primary neurons from wild-type mice (PN WT ). (F) PN WT from wild-type mice and cultured primary neurons from APP Swedish mutant transgenic mice (PN APP ) expressing human APP with the Swedish mutation were costained with anti-NLRP3 (red, Alexa Fluor 564) and anti-NeuN (green, Alexa Fluor 488) antibodies. NLRP3 was not clearly detectable beyond the background staining in PN WT , whereas the NLRP3 signal in PN APP was markedly stronger than in nonneuronal cells. Asterisks indicate nonneuronal (NeuN-negative) cells. (G) Western blot for NLRP3 in Neuro2A cell lysates. (H) Total RNA was extracted from Neuro2A cells and reverse transcribed, and the indicated genes were PCR-amplified. RNA was used as negative control template. (I) Mouse brains were lysed and treated with or without λ-protein phosphatase. The treated lysates were subjected to western blot for p-tau181 and p-tau202/205 to determine the specificity of the antibodies. PN APP were treated with the NLRP3 inhibitors CY-09 and CORM3 for 4 hours. The cell lysates were subjected to western blot for p-tau181 and p-tau202-205. Data are expressed as mean ± SD ( n = 3 independent repeats). * P < 0.05, ** P < 0.01 (one-way analysis of variance with Tukey’s post hoc test). (J) Brains lysates from APP/PS1ΔE9 mice were treated with phosphatase inhibitor (P.I.) or λ-protein phosphatase (λPP), and subjected to western blot to detect the indicated proteins. AD: Alzheimer’s disease; APP: amyloid precursor protein; DAPI: 4′,6-diamidino-2-phenylindole; DMSO: dimethyl sulfoxide; DNA: nuclear stained by DAPI that labels DNA; GSDMD: gasdermin D; GSDMD-FL: full-length GSDMD without being cleaved by active caspase-1; GSDMD-N: N-terminal fragment of GSDMD due to the cleavage of GSDMD-FL by active caspase-1; Iba1: ionized calcium binding adaptor molecule 1; NLRP3: NOD-, LRR- and pyrin domain-containing protein 3; ns: not significant; PCR: polymerase chain reaction; pro-caspase-1: The holo protein of caspase-1 without being cleaved; WT: wild-type.

Article Snippet: APPswe transgenic mice (Stock No. C001076, RRID: IMSR_JAX:001076) were purchased from Cyagen Biosciences Inc. (Suzhou, Jiangsu, China).

Techniques: Marker, Injection, Western Blot, Cell Culture, Mutagenesis, Transgenic Assay, Expressing, Staining, Reverse Transcription, Amplification, Negative Control, Binding Assay, Polymerase Chain Reaction

Journal: Neural Regeneration Research

Article Title: FUBP3 mediates the amyloid-β-induced neuronal NLRP3 expression

doi: 10.4103/NRR.NRR-D-23-01799

Figure Lengend Snippet: FUBP3 is required for NLRP3 expression in neurons in the presence of Aβ. (A) Control siRNA or mouse FUBP3 -specific siRNA and pNLRP3-Del5 were transfected into Neu2A cells for the luciferase assay. The promoter activities after normalization to the pGL3-basic vector were plotted. (B) Neuro2A cells were transfected with control siRNA or FUBP3-specific siRNA, and treated with DMSO as a control or with 1 μM Aβ overnight. The NRKP3 mRNA levels in these cells were determined by quantitative PCR, and the proteins were examined by western blot. FUBP3 and NLRP3 expression levels were quantified. (C) Primary neurons from wild-type mice (PN WT ) were infected with viruses expressing control shRNA or FUBP3 -targeting shRNA under the syn1 promoter, and treated with or without Aβ. FUBP3 and NLRP3 expression levels were compared among the different treatment groups. (D) PN WT were infected with viruses expressing control shRNA or shFUBP3, and the cells were treated with cerebrospinal fluid from patients with viral encephalitis. FUBP3 and NLRP3 were detected by western blot, and their expression levels were quantified. (E) PN APP were infected with viruses expressing control shRNA or shFUBP3, and FUBP3 and NLRP3 were detected by western blot, and their expression levels were quantified. (F) PN WT and primary neurons from APP Swedish mutant transgenic mice (PN APP ) growing on coverslips were stained with antibodies to FUBP3 (green, Alexa Fluor 488) and NeuN (red, Alexa Fluor 564), a neuronal cell marker. There was no discernable difference in FUBP3 expression levels between PN WT and PN APP . Asterisks indicate contaminating cells in the neuronal culture. (G) Brains sections from young wild-type mice, APP/PS1ΔE9 AD model mice, and aged wild-type mice were stained for FUBP3 (green, Alexa Fluor 488) and NeuN (red, Alexa Fluor 564), a neuronal marker. (H) FUBP3 was also expressed in the microglial cell line BV2. All data are expressed as mean ± SEM ( n = 3 independent repeats). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 (two-tailed Student’s t -test). Aβ: Amyloid-β; B.E.: brightness enhanced; CSF: cerebrospinal fluid; DAPI: 4′,6-diamidino-2-phenylindole; DMSO: dimethyl sulfoxide; DNA: nuclear stained by DAPI that labels DNA; FUBP3: far upstream binding protein 3; NLRP3: NOD-, LRR- and pyrin domain-containing protein 3; ns: not significant; PCR: polymerase chain reaction; shRNA: short hairpin RNA.

Article Snippet: APPswe transgenic mice (Stock No. C001076, RRID: IMSR_JAX:001076) were purchased from Cyagen Biosciences Inc. (Suzhou, Jiangsu, China).

Techniques: Expressing, Control, Transfection, Luciferase, Plasmid Preparation, Real-time Polymerase Chain Reaction, Western Blot, Infection, shRNA, Mutagenesis, Transgenic Assay, Staining, Marker, Two Tailed Test, Binding Assay, Polymerase Chain Reaction

Journal: Neural Regeneration Research

Article Title: FUBP3 mediates the amyloid-β-induced neuronal NLRP3 expression

doi: 10.4103/NRR.NRR-D-23-01799

Figure Lengend Snippet: FUBP3 is required for IL1β secretion and tau phosphorylation in PN APP . (A) PN APP were infected with AAV expressing shFUBP3 shRNA to suppress FUBP3 expression. IL1β levels in the conditioned media were determined by ELISA (PN APP from 10 different embryos). (B) PN APP were infected with AAV expressing shFUBP3 or control shRNAs. The cell lysates were subjected to western blot for indicated proteins ( n = 6). Data are expressed as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001 (two-tailed Student’s t -test). AAV: Adeno-associated virus; CaMK2α: calmodulin-dependent kinase IIα; ELISA: enzyme-linked immunosorbent assay; FUBP3: far upstream binding protein 3; IL1β: interleukin-1β; NLRP3: NOD-, LRR- and pyrin domain-containing protein 3; PME1: phosphatase methylesterase 1; PN APP : primary neurons of APP Swedish mutant single transgenic mouse; shRNA: short hairpin RNA.

Article Snippet: APPswe transgenic mice (Stock No. C001076, RRID: IMSR_JAX:001076) were purchased from Cyagen Biosciences Inc. (Suzhou, Jiangsu, China).

Techniques: Infection, Expressing, shRNA, Enzyme-linked Immunosorbent Assay, Control, Western Blot, Two Tailed Test, Virus, Binding Assay, Mutagenesis, Transgenic Assay

Journal: Neural Regeneration Research

Article Title: FUBP3 mediates the amyloid-β-induced neuronal NLRP3 expression

doi: 10.4103/NRR.NRR-D-23-01799

Figure Lengend Snippet: FUBP3 is involved in the immune response in Neuro2A cells. RNA was extracted from three paired Neuro2A cell lines expressing control- or siFUBP3-siRNA. (A) FPKM analysis of the effects of FUBP3 inhibition on gene expression compared with control cells. (B) Venn diagram showing the number of differentially expressed genes in each group. (C) PCR validation of the RNA-seq results. The expression levels of NLRP6 , GSDMD , PPP1R1A , and IL1b were examined. (D) PPP1R1A expression in primary neurons from APP Swedish mutant transgenic mice (PN APP ) in which FUBP3 was knocked down was examined by western blot ( N = 3 independent repeats, n = 5 (PN APP from five different embryos)). Data are expressed as mean ± SEM. ** P < 0.01 (two-tailed Student’s t -test). (E) KEGG analysis of key pathways highly enriched in differentially expressed genes. The red arrows indicate that genes involved in the immune response, as well as human diseases-infectious diseases viral/bacteria pathways, were highly enriched. (F) Histogram showing the number of differentially expressed genes in each KEGG pathway classification. The red arrows indicate immune system and infectious diseases (viral), and the green arrows indicate the endocrine system. (G) Gene set enrichment analysis (GSEA) using the Reactome database showed that the ATR and HDR pathways were negatively regulated in the NAF group compared with the NAC group. Aβ: Amyloid-β; DMSO: dimethyl sulfoxide; FPKM: fragments per kilobase of transcript per million fragments mapped; FUBP3: far upstream binding protein 3; GSDMD: gasdermin D; IL1b: interleukin-1b; KEGG: Kyoto Encyclopedia of Genes and Genomes; NAC: Neuro2A expressing control siRNA treated with Aβ; NAF: Neuro2A expressing siFUBP3 siRNA treated with Aβ; NDC: Neuro2A expressing control siRNA treated with DMSO; NDF: Neuro2A expressing siFUBP3 siRNA treated with DMSO; NLRP6: NOD-, LRR- and pyrin domain-containing protein 6; ns: not significant; PCR: polymerase chain reaction; PPP1R1A: protein phosphatase 1 regulatory inhibitor subunit 1A; siRNA: small interfering RNA.

Article Snippet: APPswe transgenic mice (Stock No. C001076, RRID: IMSR_JAX:001076) were purchased from Cyagen Biosciences Inc. (Suzhou, Jiangsu, China).

Techniques: Expressing, Control, Inhibition, RNA Sequencing Assay, Mutagenesis, Transgenic Assay, Western Blot, Two Tailed Test, Bacteria, Binding Assay, Polymerase Chain Reaction, Small Interfering RNA

Journal: eLife

Article Title: Tmem263 deletion disrupts the GH/IGF-1 axis and causes dwarfism and impairs skeletal acquisition

doi: 10.7554/eLife.90949

Figure Lengend Snippet: ( A ) Sequence alignment of full-length human (NP_689474), mouse (NP_001013046), chicken (NP_001006244), Xenopus frog (NP_989399), and zebrafish (NP_998306) transmembrane protein 263 (TMEM263) using Clustal-omega . Identical amino acids are shaded black and similar amino acids are shaded gray. Gaps are indicated by dash lines. The two predicted transmembrane domains are indicated in red. ( B ) TMEM263 expression across normal human tissues based on the consensus Human Protein Atlas (HPA) and Gene-Tissue Expression (GTEx) datasets. The data can be accessed via the HPA database ( https://www.proteinatlas.org ). nTPM denotes normalized protein-coding transcripts per million and it corresponds to the mean values of the different individual samples from each tissue. Bars are color-coded based on tissue groups with functional features in common. ( C ) Tmem263 expression across mouse tissues (n=11). Relative expression across tissues were first normalized to β-actin , then normalize to the tissue (pancreas) with the lowest expression. ( D ) Immunoblot analysis of cell lysate from HEK293 cells transfected with a control pCDNA3 empty plasmid or plasmid encoding human TMEM263 tagged with a C-terminal Myc-DDK epitope. Immunoblots were probed with an anti-FLAG (DDK) antibody (left panel) or an anti-TMEM263 antibody (right panel). ( E ) TMEM263 is localized to the plasma membrane. Surface biotinylation was carried out on transfected HEK293 cells. Biotinylated plasma membrane proteins were captured with Avidin-agarose beads, eluted, and immunoblotted for TMEM263 with an anti-FLAG antibody. Figure 1—source data 1. Top left – Original uncropped membrane from imager showing blue channel only as a black and white image. Two close molecular markers are noted. FLAG-tagged TMEM263 at the predicted molecular weight is marked. The cropped region used for the main figure image is marked with a dotted box. This membrane was probed with the anti-FLAG antibody. Bottom left – The same membrane as shown above, but overexposed and imaged with the light channel to show the entire membrane outline. The anti-FLAG antibody is very clean and therefore the membrane boarder is hard to see otherwise. Top right – Original uncropped membrane from imager showing blue channel only as a black and white image. Two close molecular markers are noted. FLAG-tagged TMEM263 at the predicted molecular weight is marked. The cropped region used for the main figure image is marked with a dotted box. This membrane was probed with the anti-FLAG antibody. Bottom left – The same membrane as shown above, but overexposed and imaged with the light channel to show the entire membrane outline. The anti-TMEM263 antibody is fairly clean and therefore the membrane boarder is hard to see otherwise. Figure 1—source data 2. Left – Original uncropped membrane from imager showing blue channel only as a black and white image. Two close molecular markers are noted. FLAG-tagged TMEM263 at the predicted molecular weight is marked. The cropped region used for the main figure image is marked with a dotted box. This membrane was probed with the anti-FLAG antibody. Right – The same membrane as on the left, but overexposed and imaged with the light channel to show the entire membrane outline. The anti-FLAG antibody is very clean and therefore the membrane boarder is hard to see otherwise.

Article Snippet: Strain, strain background ( Mus musculus ) , Tmem263 knockout (-/-) mouse line; C57BL/6J genetic background , This paper , , The mouse line was generated at the Johns Hopkins Transgenic Core facility. The mouse line is available upon request.

Techniques: Sequencing, Expressing, Functional Assay, Western Blot, Transfection, Control, Plasmid Preparation, Clinical Proteomics, Membrane, Avidin-Biotin Assay, Molecular Weight

Journal: eLife

Article Title: Tmem263 deletion disrupts the GH/IGF-1 axis and causes dwarfism and impairs skeletal acquisition

doi: 10.7554/eLife.90949

Figure Lengend Snippet: ( A ) Generation of Tmem263 knockout (KO) mice. The exon 3 that encodes ~81% of the full-length protein was deleted using CRISPR/Cas9 method and confirmed with DNA sequencing. The location and sequence of the two guide RNAs (gRNA) used to generate the deletion were underlined. Filled-in black boxes indicate part of the exon that codes for Tmem263 protein, and white boxes indicate part of the exon that codes for 5’ and 3’ UTR of the transcript. ( B ) Wild-type (WT) and KO alleles were confirmed by PCR genotyping. ( C ) The complete loss of Tmem263 transcript in KO mice was confirmed by qPCR in male and female mouse liver and hypothalamus (WT, n=6–8; KO, n=6–8). ( D ) The expected Mendelian versus observed genotype distributions in postnatal day 1 (P1) pups (n=82). ( E ) Representative images of WT and Tmem263 -KO pups at P1 . Milk spots are indicated by a red arrow. ( F ) Representative Alcian blue and Alizarin red staining of axial skeletal and cartilage in WT and KO P1 pups. ( G ) Body weights of WT and Tmem263 -KO pups at P1 (WT = 17; Het = 42; KO = 23), P7 (WT = 15; het = 28; KO = 5), P14 (WT = 16; het = 34; KO = 4), and P21 (WT = 33; het = 41; KO = 13). For panel G, we combined the data of male and female pups from P1 to P21. ( H ) Representative images of adult WT and Tmem263 -KO mice at 9 weeks of age. ( I–J ) Body weights and body length of WT (+/+), heterozygous (+/-), and KO (-/-) male and female mice at 9 weeks of age. Sample size for males (WT = 45; het = 73; KO = 9) and females (WT = 30; het = 59; KO = 8). ( K ) The growth curve trajectory based on the combined data in G and I. All data are presented as mean ± SEM. ****p<0.0001 (one-way ANOVA with Tukey’s multiple comparisons test).

Article Snippet: Strain, strain background ( Mus musculus ) , Tmem263 knockout (-/-) mouse line; C57BL/6J genetic background , This paper , , The mouse line was generated at the Johns Hopkins Transgenic Core facility. The mouse line is available upon request.

Techniques: Knock-Out, CRISPR, DNA Sequencing, Sequencing, Staining

Journal: eLife

Article Title: Tmem263 deletion disrupts the GH/IGF-1 axis and causes dwarfism and impairs skeletal acquisition

doi: 10.7554/eLife.90949

Figure Lengend Snippet: ( A ) Representative microCT images of bone (femur) showing a dramatic reduction in size in Tmem263 knockout (KO) (-/-) mice relative to wild-type (WT) (+/+) and heterozygous (+/-) controls at 8 weeks of age. ( B ) Femur length of WT (+/+), heterozygous (+/-), and KO (-/-) male and female mice at 8 weeks of age. ( C ) Quantification of trabecular bone volume per tissue volume (BV/TV) in the distal femur of WT (+/+), heterozygous (+/-), and KO (-/-) male and female mice. ( D ) Quantification of trabecular number (Tb. N) in the distal femur. ( E ) Trabecular bone thickness (Tb. Th). ( F ) Cortical tissue area (Tt. Ar). ( G ) Cortical area per tissue area. ( H ) Cortical thickness. ( I ) Tissue area per femur length. ( J ) Cortical thickness per femur length in male and female mice. ( K ) Representative images of tibial growth plate histology in WT and Tmem263 -KO male mice. ( L–N ) Quantification of growth plate length ( L ), proliferative zone length ( M ), and hypertrophic zone length ( N ) in WT (n=10) and KO (n=10) male mice. All data were collected on 8-week-old mice. Sample size for panels B–J: males (WT = 6; het = 6; KO = 11) and females (WT = 6; het = 6; KO = 9). All data are mean ± SE. **p<0.01; ***p<0.001; ****p<0.0001 (one-way ANOVA with Tukey’s multiple comparisons test).

Article Snippet: Strain, strain background ( Mus musculus ) , Tmem263 knockout (-/-) mouse line; C57BL/6J genetic background , This paper , , The mouse line was generated at the Johns Hopkins Transgenic Core facility. The mouse line is available upon request.

Techniques: Knock-Out

Journal: eLife

Article Title: Tmem263 deletion disrupts the GH/IGF-1 axis and causes dwarfism and impairs skeletal acquisition

doi: 10.7554/eLife.90949

Figure Lengend Snippet: Serum levels of growth hormone (GH; A ), IGF-1 ( B ), IGFBP3 ( C ), IGFALS ( D ), insulin ( E ), glucose ( F ), calcium ( G ), and phosphate ( H ) in wild-type (WT) (+/+), heterozygous (+/-), and Tmem263 -KO (-/-) male and female mice at 8 weeks of age. Sample size for panel A (GH): males (WT = 9; het = 9; KO = 5) and females (WT = 10; het = 7; KO = 8). Panel B (IGF-1): males (WT = 9; het = 9; KO = 9) and females (WT = 10; het = 7; KO = 7). Panel C (IGFBP3): males (WT = 15; het = 16; KO = 11) and females (WT = 12; het = 18; KO = 10). Panel D (IGFALS): males (WT = 10; het = 10; KO = 8) and females (WT = 10; het = 10; KO = 8). Panel E (insulin): males (WT = 12; het = 17; KO = 8) and females (WT = 10; het = 16; KO = 8). Panel F (glucose): males (WT = 9; het = 14; KO = 9) and females (WT = 6; het = 15; KO = 8). Panel G and H (calcium and phosphate): males (WT = 10; het = 10; KO = 8) and females (WT = 10; het = 10; KO = 8). ( I ) Ratio of calcium-to-phosphate in WT, heterozygous, and KO male and female mice. Sample size for males (WT = 10; het = 10; KO = 8) and females (WT = 10; het = 10; KO = 8). All data are presented as mean ± SEM. *p<0.05; **p<0.01; ***p<0.001; ****p<0.0001 (one-way ANOVA with Tukey’s multiple comparisons test).

Article Snippet: Strain, strain background ( Mus musculus ) , Tmem263 knockout (-/-) mouse line; C57BL/6J genetic background , This paper , , The mouse line was generated at the Johns Hopkins Transgenic Core facility. The mouse line is available upon request.

Techniques:

Journal: eLife

Article Title: Tmem263 deletion disrupts the GH/IGF-1 axis and causes dwarfism and impairs skeletal acquisition

doi: 10.7554/eLife.90949

Figure Lengend Snippet: ( A ) Volcano plot of male mouse liver transcriptome. ( B ) Enrichment analysis of differentially expressed genes (DEGs) by Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Reactome ( http://www.reactome.org ) databases. Plots of -Log(adj. p) vs gene ratio to show complete spread of all enrichment results for each analysis. The most effected categories are highlighted and labeled with the category name and number of up- and down-regulated genes within each. ( C ) Volcano plot showing the expression of all transcription factor (TF) genes detected in the male mouse liver transcriptome. TFs that are significantly up- or down-regulated in knockout (KO) male mouse liver are highlighted. ( D ) Heat map of DEGs involved in growth and metabolism. ( E ) Heat map of all protein-coding DEGs from the cytochrome P450 (Cyp) gene family. ( F ) Heat map of all protein-coding DEGs from the major urinary protein (Mup) gene family. ( G–I ) Tmem263 -KO male liver DEG overlap comparison to three separate public datasets of mouse liver gene expression: ( G ) wild-type (WT) male vs. WT female mice , ( H ) hypophysectomized vs. sham control male mice , and ( I ) Stat5b -KO vs WT male mice . ( J ) Summary of key findings underpinning the dwarfism and skeletal dysplasia phenotypes of Tmem263-null mice. All heat map data is shown on a column z-score scale. Only significantly different genes (adjusted p-value <0.05 and Log 2 (FC) <-1 or >1) are shown for all heat maps. PCG = protein-coding gene, NPCG = non-protein-coding gene. Sample size for male WT (n=8) and KO (n=8) mice (9-week-old) in all data shown.

Article Snippet: Strain, strain background ( Mus musculus ) , Tmem263 knockout (-/-) mouse line; C57BL/6J genetic background , This paper , , The mouse line was generated at the Johns Hopkins Transgenic Core facility. The mouse line is available upon request.

Techniques: Labeling, Expressing, Knock-Out, Comparison, Gene Expression, Control

Journal: eLife

Article Title: Tmem263 deletion disrupts the GH/IGF-1 axis and causes dwarfism and impairs skeletal acquisition

doi: 10.7554/eLife.90949

Figure Lengend Snippet: The DEGs from Tmem263 (-/-) male mouse liver compared to the published DEGs from (i) wild-type (WT) male vs female mice (M/F), (ii) hypophysectomized vs sham control male mice (Hypox), and (iii) Stat5b -KO vs WT male mice (Stat5b-/-). ( A–B ) All Tmem263 -KO male liver up-regulated ( A ) and down-regulated ( B ) genes considered a DEG in at least one other experiment. A red box indicates the gene is up-regulated within the given experiment, a blue box indicates down-regulation within the experiment, and a gray box indicates that the particular gene is not a DEG in the given experiment.

Article Snippet: Strain, strain background ( Mus musculus ) , Tmem263 knockout (-/-) mouse line; C57BL/6J genetic background , This paper , , The mouse line was generated at the Johns Hopkins Transgenic Core facility. The mouse line is available upon request.

Techniques: Control

Journal: eLife

Article Title: Tmem263 deletion disrupts the GH/IGF-1 axis and causes dwarfism and impairs skeletal acquisition

doi: 10.7554/eLife.90949

Figure Lengend Snippet:

Article Snippet: Strain, strain background ( Mus musculus ) , Tmem263 knockout (-/-) mouse line; C57BL/6J genetic background , This paper , , The mouse line was generated at the Johns Hopkins Transgenic Core facility. The mouse line is available upon request.

Techniques: Knock-Out, Generated, Transgenic Assay, Transfection, Construct, Expressing, Plasmid Preparation, FLAG-tag, Recombinant, Injection, Isolation, Enzyme-linked Immunosorbent Assay, cDNA Synthesis, SYBR Green Assay