Journal: International Journal of Molecular Sciences

Article Title: Nidogen 2 Overexpression Promotes Hepatosteatosis and Atherosclerosis

doi: 10.3390/ijms252312782

Figure Lengend Snippet: Expression of NID2 protein is elevated in human atherosclerotic arteries and murine steatotic livers. ( A ) Representative western blot images for NID2 and β-tubulin protein expression in human atherosclerotic inner curvature (IC) and non-atherosclerotic descending aorta (DA) vascular tissue. The bar diagram shows mean protein levels expressed as a ratio of NID2 to β-tubulin. ( B ) Representative Western blot images for NID2 (red arrowhead points to the correct band) and GAPDH in the livers of control diet (CD)- and calorie-matched high-fat diet (HFD, 12 weeks)-fed C57BL/6J mice. The bar diagram represents the mean NID2 protein expression ( n = 4). Statistical analyses were performed using a two-tailed unpaired t -test ( A , B ). Data represent mean ± SEM. * p < 0.05, and **** p < 0.0001.

Article Snippet: The following primary antibodies were used: NID2 (Proteintech, Rosemont, IL, USA #13530-1-AP), total ACC (Cell Signaling Technology, Danvers, MA, USA, #3662S), pACC Ser79 (Cell Signaling Technology, Danvers, MA, USA, #11818S), total AMPKα (Cell Signaling Technology, Danvers, MA, USA, #2793S), pAMPKα Thr172 (Cell Signaling Technology, Danvers, MA, USA, #2535S), IL-6 (Cell Signaling Technology, Danvers, MA, USA, #12912S), TNFα (Cell Signaling Technology, Danvers, MA, USA, #11948T), β-Tubulin (Cell Signaling Technology, Danvers, MA, USA, #86298S), and GAPDH (Santa Cruz Biotechnology, Dallas, TX, USA #sc-365062).

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

Journal: International Journal of Molecular Sciences

Article Title: Nidogen 2 Overexpression Promotes Hepatosteatosis and Atherosclerosis

doi: 10.3390/ijms252312782

Figure Lengend Snippet: NID2 overexpression enhances liver and epididymal white adipose tissue mass in male mice. ( A ) The schematic diagram illustrates the experimental plan. Apoe −/− mice were injected with control (Ctrl) and NID2 -AAV intraperitoneally, fed a Western diet for 12 weeks, and analyzed. ( B – E ) Male control and NID2 -AAV-injected Apoe −/− mice were utilized to measure NID2 mRNA levels in various organs by qRT-PCR at least in duplicate. Bar diagrams represent mRNA expression in the liver ( B , n = 10), kidney ( C , n = 6), epididymal white adipose tissue (EpiWAT, D , n = 7–10), and heart ( E , n = 10). Bar diagrams show body weight gain ( F ), plasma total cholesterol ( G ), fasting blood glucose ( H ), whole-body fat/lean mass ( I ), liver weight ( J ), adipose tissue weight ( K ), and spleen weight ( L ) ( n = 5–6). A two-tailed unpaired t -test ( C , G – K ), two-tailed unpaired Mann–Whitney test ( B , D , E , L ), and two-way ANOVA followed by Sidak post hoc test for multiple comparisons ( F ) were utilized for statistical analyses. Data represent mean ± SEM. ns: non-significant. * p < 0.05, *** p < 0.001 and **** p < 0.0001.

Article Snippet: The following primary antibodies were used: NID2 (Proteintech, Rosemont, IL, USA #13530-1-AP), total ACC (Cell Signaling Technology, Danvers, MA, USA, #3662S), pACC Ser79 (Cell Signaling Technology, Danvers, MA, USA, #11818S), total AMPKα (Cell Signaling Technology, Danvers, MA, USA, #2793S), pAMPKα Thr172 (Cell Signaling Technology, Danvers, MA, USA, #2535S), IL-6 (Cell Signaling Technology, Danvers, MA, USA, #12912S), TNFα (Cell Signaling Technology, Danvers, MA, USA, #11948T), β-Tubulin (Cell Signaling Technology, Danvers, MA, USA, #86298S), and GAPDH (Santa Cruz Biotechnology, Dallas, TX, USA #sc-365062).

Techniques: Over Expression, Injection, Control, Western Blot, Quantitative RT-PCR, Expressing, Clinical Proteomics, Two Tailed Test, MANN-WHITNEY

Journal: International Journal of Molecular Sciences

Article Title: Nidogen 2 Overexpression Promotes Hepatosteatosis and Atherosclerosis

doi: 10.3390/ijms252312782

Figure Lengend Snippet: NID2 overexpression in mice promotes hepatic lipid accumulation and fibrosis. Male Apoe −/− mice were injected with control and NID2 -AAV intraperitoneally, fed a Western diet for 12 weeks, and analyzed. ( A ) Representative Western blot images for NID2 and GAPDH protein expression in the livers of control and NID2 -overexpressing mice ( n = 3). ( B ) Representative images of liver sections stained with H & E (lipid droplets), ORO (neutral lipid accumulation), and Sirius red (fibrosis); scale bar 100 μm. ( C – H ) Bar diagrams represent lipid accumulation ( C , n = 6), fibrosis area ( D , n = 5), hepatic triglyceride ( E , n = 3–4), NEFA levels ( F , n = 3–4), plasma triglyceride ( G , n = 5) and NEFA levels ( H , n = 5), in control and NID2 -AAV-injected mice. Statistical analyses were performed using a two-tailed unpaired t -test ( C – H ). Data represent mean ± SEM. ns: non-significant. * p < 0.05, and ** p < 0.01.

Article Snippet: The following primary antibodies were used: NID2 (Proteintech, Rosemont, IL, USA #13530-1-AP), total ACC (Cell Signaling Technology, Danvers, MA, USA, #3662S), pACC Ser79 (Cell Signaling Technology, Danvers, MA, USA, #11818S), total AMPKα (Cell Signaling Technology, Danvers, MA, USA, #2793S), pAMPKα Thr172 (Cell Signaling Technology, Danvers, MA, USA, #2535S), IL-6 (Cell Signaling Technology, Danvers, MA, USA, #12912S), TNFα (Cell Signaling Technology, Danvers, MA, USA, #11948T), β-Tubulin (Cell Signaling Technology, Danvers, MA, USA, #86298S), and GAPDH (Santa Cruz Biotechnology, Dallas, TX, USA #sc-365062).

Techniques: Over Expression, Injection, Control, Western Blot, Expressing, Staining, Clinical Proteomics, Two Tailed Test

Journal: International Journal of Molecular Sciences

Article Title: Nidogen 2 Overexpression Promotes Hepatosteatosis and Atherosclerosis

doi: 10.3390/ijms252312782

Figure Lengend Snippet: NID2 overexpression augments atherosclerosis in male hypercholesterolemic mice. Male Apoe −/− mice were injected with control (Ctrl) and NID2 -AAV intraperitoneally, fed a Western diet for 12 weeks and analyzed. ( A ) Representative in situ images of the aortic arch (red arrowheads point to atherosclerotic lesions). ( B ) Representative ORO staining of whole aortas; scale bar 5 mm. The bar diagram represents ORO-positive areas in whole aortas ( n = 6). ( C ) Representative images of aortic root cross-sections stained with H & E (lesion area and necrotic core), ORO (lipid accumulation), and Masson’s trichrome (collagen content); scale bar 200 μm. ( D – G ) Bar diagrams show lesion area ( D ), lipid deposition ( E ), collagen content ( F ), and necrotic core area ( G ) ( n = 5–6). Statistical analyses were performed using a two-tailed unpaired t -test ( B , D – G ). Data represent mean ± SEM. * p < 0.05, and ** p < 0.01.

Article Snippet: The following primary antibodies were used: NID2 (Proteintech, Rosemont, IL, USA #13530-1-AP), total ACC (Cell Signaling Technology, Danvers, MA, USA, #3662S), pACC Ser79 (Cell Signaling Technology, Danvers, MA, USA, #11818S), total AMPKα (Cell Signaling Technology, Danvers, MA, USA, #2793S), pAMPKα Thr172 (Cell Signaling Technology, Danvers, MA, USA, #2535S), IL-6 (Cell Signaling Technology, Danvers, MA, USA, #12912S), TNFα (Cell Signaling Technology, Danvers, MA, USA, #11948T), β-Tubulin (Cell Signaling Technology, Danvers, MA, USA, #86298S), and GAPDH (Santa Cruz Biotechnology, Dallas, TX, USA #sc-365062).

Techniques: Over Expression, Injection, Control, Western Blot, In Situ, Staining, Two Tailed Test

Journal: International Journal of Molecular Sciences

Article Title: Nidogen 2 Overexpression Promotes Hepatosteatosis and Atherosclerosis

doi: 10.3390/ijms252312782

Figure Lengend Snippet: NID2 overexpression inhibits the activation of the lipid metabolism-related protein AMPK. ( A ) Representative Western blot images for lipid metabolism and pro-inflammatory proteins utilizing liver lysates from control and NID2 -AAV-injected mice. Bar diagrams represent mean protein expression ( B , C ) as the ratios of phospho-total proteins ACC ( B ) and AMPK ( C ), and protein levels of IL-6 ( D ) and TNFα ( E ) ( n = 5). Statistical analyses were performed using a two-tailed unpaired t -test. Data represent mean ± SEM. ns: non-significant. * p < 0.05.

Article Snippet: The following primary antibodies were used: NID2 (Proteintech, Rosemont, IL, USA #13530-1-AP), total ACC (Cell Signaling Technology, Danvers, MA, USA, #3662S), pACC Ser79 (Cell Signaling Technology, Danvers, MA, USA, #11818S), total AMPKα (Cell Signaling Technology, Danvers, MA, USA, #2793S), pAMPKα Thr172 (Cell Signaling Technology, Danvers, MA, USA, #2535S), IL-6 (Cell Signaling Technology, Danvers, MA, USA, #12912S), TNFα (Cell Signaling Technology, Danvers, MA, USA, #11948T), β-Tubulin (Cell Signaling Technology, Danvers, MA, USA, #86298S), and GAPDH (Santa Cruz Biotechnology, Dallas, TX, USA #sc-365062).

Techniques: Over Expression, Activation Assay, Western Blot, Control, Injection, Expressing, Two Tailed Test

Journal: Molecular Human Reproduction

Article Title: Upregulated TIMP1 facilitates and coordinates myometrial contraction by decreasing collagens and cell adhesive capacity during human labor

doi: 10.1093/molehr/gaad034

Figure Lengend Snippet: Different cell adhesive properties in different human myometrial smooth muscle cells (hMSMCs). ( A ) Cell adhesive properties in nonpregnant, nonlabor and in-labor term hMSMCs. *IL versus NL, P < 0.05. ( B ) Cell adhesion properties in laboring hMSMCs with/without si-TIMP1 or oe-TIMP1. *si-TIMP1 versus the control, P < 0.05. ( C ) Representative western blotting of SPP1 (70 kDa), NID2 (151 kDa), and VCAN (373 kDa) in laboring hMSMCs with/without si-TIMP1 knockdown. See for full western blots. ( D ) Ratio of SPP1, NID2, and VCAN/β-actin expression in western blotting. ( E ) RNA-seq analysis shows the mRNA expression before and after si-TIMP1 knockdown. TIMP1, tissue inhibitor of metalloproteinase 1; SPP1, osteopontin; NID2, nidogen-2; VCAN, versican; NL, nonlabor; IL, in-labor. Data are presented as mean ± SEM from 3 to 10 independent experiments. * P < 0.05.

Article Snippet: The antibodies used were rabbit polyclonal β-actin antibody (1:5000, ab8226, Abcam, Cambridge, UK), rabbit monoclonal TIMP1 antibody (1:1000, ab211926, Abcam, Cambridge, UK), rabbit polyclonal NID2 (1:1000, DF9704, Affinity Biosciences, Changzhou, China), rabbit monoclonal VCAN (1:1000, ab270444, Abcam, Cambridge, UK), rabbit polyclonal SPP1 (1:1000, GB112328, Servicebio, Wuhan, China), and rabbit polyclonal GAPDH (1:1000, AF7021, Affinity Biosciences, Changzhou, China).

Techniques: Adhesive, Control, Western Blot, Knockdown, Expressing, RNA Sequencing

Journal: Neural Development

Article Title: A synaptic nidogen: Developmental regulation and role of nidogen-2 at the neuromuscular junction

doi: 10.1186/1749-8104-3-24

Figure Lengend Snippet: Nidogen isoforms are differentially expressed in mouse muscle. (A, B) Western blotting of recombinant nidogen-1 (N1) and -2 (N2) demonstrates specificity of nidogen-1 and nidogen-2 antibodies. (C, D) Young adult (postnatal day 56) mouse muscle cross-sectioned and immunostained with anti-nidogen-1 (C) or anti-nidogen-2 (D) antibodies. Nidogen-1 is present in the basal lamina surrounding muscle fibers. Nidogen-2 is largely absent from muscle fiber basal lamina, but is present in discrete basal laminas within muscle. (E, E') Double labeling of muscle with α-bungarotoxin (E) and anti-nidogen-2 (E') reveals that nidogen-2 is present at acetylcholine receptor-rich synaptic sites (arrows). Scale bar is 25 μm.

Article Snippet: They are: nidogen-2 mutants ( nid2 -/- ) [ ], laminin β2 mutants ( lamb2 -/- ) [ ], laminin α4 mutants ( lama4 -/- ) [ ], collagen α5(IV) mutants ( col4a5 -/ Y ) [ ], obtained from Jackson Laboratories, Bar Harbor, ME, USA), conditional laminin α5 mutants ( lama5 flox / flox ) [ ], and mice that express Cre selectively in skeletal muscle (HSA-Cre) [ ].

Techniques: Western Blot, Recombinant, Labeling

Journal: Neural Development

Article Title: A synaptic nidogen: Developmental regulation and role of nidogen-2 at the neuromuscular junction

doi: 10.1186/1749-8104-3-24

Figure Lengend Snippet: Differential distribution of nidogens at the neuromuscular junction (NMJ). (A) Schematic representation of the three cellular components of the NMJ (motor nerve terminal (NT), peri-synaptic Schwann cell process (SC), and skeletal muscle fibers (M)) and the basal laminas (BLs) that coat them (dashed lines). Dashed lines: red, synaptic BL; blue, extrasynaptic BL; green, Schwann cell BL. (B-C") Young adult NMJ cross-sections costained with α-bungarotoxin (BTX) and either anti-nidogen-1 (B) or anti-nidogen-2 (C). Nidogen-1 is present in synaptic, extrasynaptic (arrows in B', B") and Schwann cell BLs (arrowheads in B', B"). Nidogen-2 is absent extrasynaptically, but is enriched in synaptic and Schwann cell BLs (arrowheads in C', C"). (D-D") Confocal, en face image of an NMJ double-stained with BTX and anti-nidogen-2. Regions of co-localization demonstrate nidogen-2-rich synaptic BL. Tube-like structures overlaying synaptic sites (arrowheads) represent Schwann cell BL. Nidogen-2-positive structures near synaptic sites are capillaries (asterisks). (E-E") Nidogen-2 localized to acetylcholine receptor-rich (BTX-stained) sites in C2C12 myotubes. Scale bars are 5 μm in (B, C) and 20 μm in (D, E).

Article Snippet: They are: nidogen-2 mutants ( nid2 -/- ) [ ], laminin β2 mutants ( lamb2 -/- ) [ ], laminin α4 mutants ( lama4 -/- ) [ ], collagen α5(IV) mutants ( col4a5 -/ Y ) [ ], obtained from Jackson Laboratories, Bar Harbor, ME, USA), conditional laminin α5 mutants ( lama5 flox / flox ) [ ], and mice that express Cre selectively in skeletal muscle (HSA-Cre) [ ].

Techniques: Staining

Journal: Neural Development

Article Title: A synaptic nidogen: Developmental regulation and role of nidogen-2 at the neuromuscular junction

doi: 10.1186/1749-8104-3-24

Figure Lengend Snippet: Differential localization of nidogen isoforms in peripheral nerve. (A, B) Nidogens are differentially localized in the basal laminas (BLs) associated with intramuscular nerve fascicles. Whereas nidogen-1 is present at similar levels in both peri- and endoneurial BL, nidogen-2 is enriched in perineurial BL. Most endoneurial BL expressed little nidogen-2, but a few structures within the nerve fascicle did contain nidogen-2 (arrowheads). Double staining with antibodies to CD31/PECAM indicate that most nidogen-2-positive structures within nerve fascicles are not associated with capillaries (data not shown). (C, D) Nidogens are differentially localized in BLs associated with sensory muscle spindles. Nidogen-1 is enriched in BLs surrounding individual intrafusal fibers within the muscle spindle, but nidogen-2 is enriched in the capsular BL surrounding the entire spindle. (E-H) Nidogen-1 and 2 are both present in BLs associated with vascular structures, including capillaries (E, F; arrowheads in E, G, H highlight capillary BL) and arterioles (arrows in G, H). Scale bar in (B) is 20 μm for (A, B), in (D) is 10 μm for (C, D), in (F) is 20 μm for (E, F), and in (H) is 20 μm for (G, H).

Article Snippet: They are: nidogen-2 mutants ( nid2 -/- ) [ ], laminin β2 mutants ( lamb2 -/- ) [ ], laminin α4 mutants ( lama4 -/- ) [ ], collagen α5(IV) mutants ( col4a5 -/ Y ) [ ], obtained from Jackson Laboratories, Bar Harbor, ME, USA), conditional laminin α5 mutants ( lama5 flox / flox ) [ ], and mice that express Cre selectively in skeletal muscle (HSA-Cre) [ ].

Techniques: Double Staining

Journal: Neural Development

Article Title: A synaptic nidogen: Developmental regulation and role of nidogen-2 at the neuromuscular junction

doi: 10.1186/1749-8104-3-24

Figure Lengend Snippet: Developmental regulation of nidogens and laminin α chains in synaptic basal lamina (BL). Cross-sections of muscle from P0 (A, D, G, J), P14 (B, E, H, K) and P21 (C, F, I, L) mice, stained for α-bungarotoxin (BTX) and nidogens or laminins. (A-F) While nidogen-1 expression changes little during development (A-C), nidogen-2 is present in both synaptic and extrasynaptic BLs at birth (D) and becomes restricted to synaptic BL postnatally (E, F). (G-L) Laminins α4 (G-I) and α5 (J-L) become restricted to synaptic BL in parallel with nidogen-2. Scale bar is 15 μm for (A, D, G, J) and 10 μm for all other panels.

Article Snippet: They are: nidogen-2 mutants ( nid2 -/- ) [ ], laminin β2 mutants ( lamb2 -/- ) [ ], laminin α4 mutants ( lama4 -/- ) [ ], collagen α5(IV) mutants ( col4a5 -/ Y ) [ ], obtained from Jackson Laboratories, Bar Harbor, ME, USA), conditional laminin α5 mutants ( lama5 flox / flox ) [ ], and mice that express Cre selectively in skeletal muscle (HSA-Cre) [ ].

Techniques: Staining, Expressing

Journal: Neural Development

Article Title: A synaptic nidogen: Developmental regulation and role of nidogen-2 at the neuromuscular junction

doi: 10.1186/1749-8104-3-24

Figure Lengend Snippet: Aberrant neuromuscular junction (NMJ) morphology in the absence of nidogen-2. NMJs from diaphragms of P56 nid2 -/- mutants and aged-matched controls. Pre- and postsynaptic elements are labeled with anti-synaptotagmin 2 (syt 2) and α-bungarotoxin (BTX). (A) In controls, NMJs appeared pretzel-like. (B-E) In mutants, NMJs were frequently fragmented into small clusters (B, D, E) or appeared plaque-like (C). Despite topological abnormalities, mutant pre- and postsynaptic elements remain precisely aligned (B"). Scale bar in (A) is 10 μm for all parts.

Article Snippet: They are: nidogen-2 mutants ( nid2 -/- ) [ ], laminin β2 mutants ( lamb2 -/- ) [ ], laminin α4 mutants ( lama4 -/- ) [ ], collagen α5(IV) mutants ( col4a5 -/ Y ) [ ], obtained from Jackson Laboratories, Bar Harbor, ME, USA), conditional laminin α5 mutants ( lama5 flox / flox ) [ ], and mice that express Cre selectively in skeletal muscle (HSA-Cre) [ ].

Techniques: Labeling, Mutagenesis

Journal: Neural Development

Article Title: A synaptic nidogen: Developmental regulation and role of nidogen-2 at the neuromuscular junction

doi: 10.1186/1749-8104-3-24

Figure Lengend Snippet: Morphological defects in nid2 -/- neuromuscular junctions (NMJs) are due to improper maturation and maintenance. (A, B) NMJs from diaphragms of P7 (A) and P21 (B) nid2 -/- mutants and aged-matched controls. Pre- and postsynaptic elements are labeled with anti-synaptotagmin 2 antibodies (syt 2) and α-bungarotoxin (BTX), respectively. No obvious defects were present at either age. (C) NMJs from diaphragms of 1-year-old mutants and age-matched controls. Mutant NMJs were fragmented at 1 year of age but were not appreciably more severely affected than in 2-month-old mutants (Figure 5). Scale bars are 20 μm.

Article Snippet: They are: nidogen-2 mutants ( nid2 -/- ) [ ], laminin β2 mutants ( lamb2 -/- ) [ ], laminin α4 mutants ( lama4 -/- ) [ ], collagen α5(IV) mutants ( col4a5 -/ Y ) [ ], obtained from Jackson Laboratories, Bar Harbor, ME, USA), conditional laminin α5 mutants ( lama5 flox / flox ) [ ], and mice that express Cre selectively in skeletal muscle (HSA-Cre) [ ].

Techniques: Labeling, Mutagenesis

Journal: Neural Development

Article Title: A synaptic nidogen: Developmental regulation and role of nidogen-2 at the neuromuscular junction

doi: 10.1186/1749-8104-3-24

Figure Lengend Snippet: Nidogen-2 is not required to restrict other basal lamina (BL) components to the synaptic BL. (A-J) Synaptic sites in P56 nid2 -/- muscle cross sections were labeled with α-bungarotoxin (BTX) and antibodies to BL components: nidogen-1 (B) and -2 (A), synaptic laminin chains (Lamα4 [C], Lamα5 [D], and Lamβ2 [E] chains), agrin (F), and synaptic collagens IV (Colα3–6 [IV]) (G-J). No other components of the synaptic BL appeared altered in the absence of nidogen-2. Scale bar is 10 μm.

Article Snippet: They are: nidogen-2 mutants ( nid2 -/- ) [ ], laminin β2 mutants ( lamb2 -/- ) [ ], laminin α4 mutants ( lama4 -/- ) [ ], collagen α5(IV) mutants ( col4a5 -/ Y ) [ ], obtained from Jackson Laboratories, Bar Harbor, ME, USA), conditional laminin α5 mutants ( lama5 flox / flox ) [ ], and mice that express Cre selectively in skeletal muscle (HSA-Cre) [ ].

Techniques: Labeling

Journal: Neural Development

Article Title: A synaptic nidogen: Developmental regulation and role of nidogen-2 at the neuromuscular junction

doi: 10.1186/1749-8104-3-24

Figure Lengend Snippet: Nidogen-2 phenotypes vary among muscles. (A-C) Neuromuscular junction (NMJ) morphology was differentially affected in different muscles. Like diaphragm (Dia) (A), most NMJs in soleus (Sol) muscles were fragmented or immature (B), whereas NMJs in tibialis anterior (TA) and extensor digitorum longus (EDL) appeared less affected (C, D). NMJs were labeled with only α-bungarotoxin. (E) Quantification of NMJ morphology in several different mutant and control muscles. Y-axis represents the percentage of NMJs appearing either pretzel-like (that is, normal), fragmented (blue, as in Figure 6B, D, E), or immature (red, as in Figure 6C). Control tibialis anterior, n = 92 NMJs from 3 animals. Control diaphragm, n = 100 NMJs from 3 animals. Nid2 -/- EDL, n = 105, from 3 animals. Nid2 -/- tibialis anterior, n = 91, from 3 animals. Nid2 -/- soleus, n = 129, from 3 animals. Nid2 -/- diaphragm; n = 384, from 3 animals. Scale bar in (D) is 25 μm for (A-D).

Article Snippet: They are: nidogen-2 mutants ( nid2 -/- ) [ ], laminin β2 mutants ( lamb2 -/- ) [ ], laminin α4 mutants ( lama4 -/- ) [ ], collagen α5(IV) mutants ( col4a5 -/ Y ) [ ], obtained from Jackson Laboratories, Bar Harbor, ME, USA), conditional laminin α5 mutants ( lama5 flox / flox ) [ ], and mice that express Cre selectively in skeletal muscle (HSA-Cre) [ ].

Techniques: Muscles, Labeling, Mutagenesis, Control

Journal: Neural Development

Article Title: A synaptic nidogen: Developmental regulation and role of nidogen-2 at the neuromuscular junction

doi: 10.1186/1749-8104-3-24

Figure Lengend Snippet: Nidogen-2 localized to synaptic sites in the absence of other synaptic basal lamina components. (A-E) Nidogen-2 was properly localized at synaptic sites (labeled with α-bungarotoxin (BTX)) in mutant mice lacking laminin α4 ( lama4 -/- ) (A), laminin α5 ( lama5 M/M :HSA-Cre) (B), both laminin α4 and α5 ( lama4 -/- ; lama5 M/M : HSA -Cre) (C), laminin β2 ( lamb2 -/- ) (D) and all four synaptic collagen IV chains ( col4a5 -/Y ) (E). Scale bar is 5 μm.

Article Snippet: They are: nidogen-2 mutants ( nid2 -/- ) [ ], laminin β2 mutants ( lamb2 -/- ) [ ], laminin α4 mutants ( lama4 -/- ) [ ], collagen α5(IV) mutants ( col4a5 -/ Y ) [ ], obtained from Jackson Laboratories, Bar Harbor, ME, USA), conditional laminin α5 mutants ( lama5 flox / flox ) [ ], and mice that express Cre selectively in skeletal muscle (HSA-Cre) [ ].

Techniques: Labeling, Mutagenesis

Journal: Neural Development

Article Title: A synaptic nidogen: Developmental regulation and role of nidogen-2 at the neuromuscular junction

doi: 10.1186/1749-8104-3-24

Figure Lengend Snippet: Synaptic localization of laminins, collagens IV and agrin occurs independently of other major basal lamina (BL) components. (A-G) In addition to nidogen-2 (Figure 9) other components of synaptic BL were examined in mutant mice lacking all four synaptic collagen IV chains ( col4a5 -/Y ) (A-D) and collagen α3(IV) in laminin β2 ( lamb2 -/- ) (E), laminin α4 ( lama4 -/- ) (F) and laminin α5 ( lama5 M/M : HAS -Cre) (G) mutants. In the absence of any synaptic BL component, other families of BL molecules remained properly enriched at synaptic sites. Scale bar is 5 μm.

Article Snippet: They are: nidogen-2 mutants ( nid2 -/- ) [ ], laminin β2 mutants ( lamb2 -/- ) [ ], laminin α4 mutants ( lama4 -/- ) [ ], collagen α5(IV) mutants ( col4a5 -/ Y ) [ ], obtained from Jackson Laboratories, Bar Harbor, ME, USA), conditional laminin α5 mutants ( lama5 flox / flox ) [ ], and mice that express Cre selectively in skeletal muscle (HSA-Cre) [ ].

Techniques: Mutagenesis

Journal: Neural Development

Article Title: A synaptic nidogen: Developmental regulation and role of nidogen-2 at the neuromuscular junction

doi: 10.1186/1749-8104-3-24

Figure Lengend Snippet: Enrichment of laminins, collagens IV, nidogen 2 and agrin in synaptic basal lamina of mutant mice

Article Snippet: They are: nidogen-2 mutants ( nid2 -/- ) [ ], laminin β2 mutants ( lamb2 -/- ) [ ], laminin α4 mutants ( lama4 -/- ) [ ], collagen α5(IV) mutants ( col4a5 -/ Y ) [ ], obtained from Jackson Laboratories, Bar Harbor, ME, USA), conditional laminin α5 mutants ( lama5 flox / flox ) [ ], and mice that express Cre selectively in skeletal muscle (HSA-Cre) [ ].

Techniques: Mutagenesis