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Novus Biologicals stathmin 2 stmn2
Antibodies/Reagent used for immunofluorescence staining.

Stathmin 2 Stmn2, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/stmn2/Stathmin-2%2FSTMN2+Antibody+%5BPE%5D/pmc10076424-2-0-7
Average 91 stars, based on 1 article reviews

stathmin 2 stmn2 - by Bioz Stars, 2026-10

91/100 stars

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1) Product Images from "Enhanced axonal regeneration of ALS patient iPSC-derived motor neurons harboring SOD1 A4V mutation"

Article Title: Enhanced axonal regeneration of ALS patient iPSC-derived motor neurons harboring SOD1 A4V mutation

Journal: Scientific Reports

doi: 10.1038/s41598-023-31720-7

Figure Legend Snippet: Antibodies/Reagent used for immunofluorescence staining.

Techniques Used: Immunofluorescence, Staining, Marker

$SOD1 +/+ and SOD1 +/A4V axons regenerate similarly 24 h following axotomy. ( A ) Mean axon length 24 h post-axotomy (SOD1 +/+ n = 13; SOD1 +/A4V n = 12). Each data point represents 50–100 traced axons from 1 individual axonal compartment. ( B ) Frequency distribution of axon length 24 h post-axotomy. ( C ) SOD1 +/+ (left) and SOD1 +/A4V (right) regenerating axons 24 h post axotomy stained for GAP-43. Scale bar = 50 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\upmu$$\end{document} μ m. ( D-E ) Growth cones 24 h post axotomy stained for smi-31 (green), F-actin (white), stathmin-2 (red). Scale bar = 2 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\upmu$$\end{document} μ m. ( D ) SOD1 +/+ (top panels) ( E ) SOD1 +/A4V (bottom panels). ( F ) Average growth cone area 24 h post-axotomy. (G) Average STMN2 fluorescence intensity in growth cone area 24 h post-axotomy. Bars represent mean ± SEM. ns indicates p > 0.05.$
Figure Legend Snippet: SOD1 +/+ and SOD1 +/A4V axons regenerate similarly 24 h following axotomy. ( A ) Mean axon length 24 h post-axotomy (SOD1 +/+ n = 13; SOD1 +/A4V n = 12). Each data point represents 50–100 traced axons from 1 individual axonal compartment. ( B ) Frequency distribution of axon length 24 h post-axotomy. ( C ) SOD1 +/+ (left) and SOD1 +/A4V (right) regenerating axons 24 h post axotomy stained for GAP-43. Scale bar = 50 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\upmu$$\end{document} μ m. ( D-E ) Growth cones 24 h post axotomy stained for smi-31 (green), F-actin (white), stathmin-2 (red). Scale bar = 2 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\upmu$$\end{document} μ m. ( D ) SOD1 +/+ (top panels) ( E ) SOD1 +/A4V (bottom panels). ( F ) Average growth cone area 24 h post-axotomy. (G) Average STMN2 fluorescence intensity in growth cone area 24 h post-axotomy. Bars represent mean ± SEM. ns indicates p > 0.05.

Techniques Used: Staining, Fluorescence

Marker:

Article Title: Enhanced axonal regeneration of ALS patient iPSC-derived motor neurons harboring SOD1 A4V mutation
Article Snippet: β3-tubulin (TUBB3) , Neuronal marker , Biolegend , 1:2000. .. Stathmin-2 (STMN2) , Early regeneration marker , Novus , 1:2000. .. GAP-43 , Regeneration Marker , Sigma-Aldrich , 1:1000.

Image Search Results

( A ) Single-step (MOI 5) replication curve of wildtype (WT) and ΔpUL56 HSV-1 in day 14 i3Neurones. Mean ± SD for three independent experiments is shown. ( B ) Schematic of the QTV workflow using day 14 i3Neurones. Mock samples were harvested at 12 hpi for all analyses, and additionally at 3 and 30 hpi for transcriptomics (RNAseq) using Oxford Nanopore Technology (ONT). ( C ) Changes in i3Neurone protein abundance at 30 hpi with WT HSV-1. Horizontal axis shows average fold change and vertical axis shows significance (two-sided t-test) for three independent experiments. Proteins are coloured by FDR-corrected significance and viral proteins are outlined in pink. ( D ) Changes in i3Neurone transcript abundance at 30 hpi with WT HSV-1. Horizontal axis shows average fold change and vertical axis shows FDR-adjusted significance for three independent experiments. Significantly altered genes (log 2 fold change ≥ 2 and p ≤ 0.05) are blue and viral transcripts are outlined in pink. ( E ) Immunoblot analysis of day 14 i3Neurones at 16 hpi (MOI 10) with HSV-1 strains KOS, S17 and SC16, or Semliki Forest virus (SFV)4. Changes in KIF1A, cFOS and GOPC are HSV-1 specific, whereas abundance of stathmins (STMN2–4) is altered in all infections. Capsid proteins VP5 (HSV) and CP (SFV4) confirm successful infection and GAPDH is a loading control. ( F ) Gene Ontology (GO) analysis of proteins (top, blue) and transcripts (bottom, green) with significantly changed abundance at 30 hpi in HSV-versus mock-infected i3Neurones. Significant GO molecular function terms are shown as bubbles sized by magnitude of enrichment, with significance (FDR-adjusted p-value) plotted on the horizontal axis and arrows indicating whether the term was enriched amongst the up- or down-regulated gene products. ( G ) Changes in protein (horizontal) versus transcript (vertical) abundance in mock-versus HSV-infected i3Neurones at 30 hpi. Cellular and viral gene products are grey and pink, respectively, with selected cellular gene products highlighted (black). Potential targets of HSV-1 directed proteasomal degradation (larger fold change in protein vs transcript abundance) are to the left of the dotted red line. (H) Normalised abundance traces of selected proteins (top) and transcripts (bottom) across the time course of infection with WT (pink) or ΔpUL56 (blue) HSV-1. Mock-infected samples (M) are shown as 0 hpi. ( I ) Cellular protein abundance changes in day 14 i3Neurones infected (MOI 5) with WT versus ΔpUL56 i3Neurones. Data are plotted as in ( C ), with horizontal axis showing average mock-corrected fold change for three independent experiments.

Journal: bioRxiv

Article Title: Herpes simplex virus pUL56 abolishes neuronal activity by removing voltage-gated ion channels from the plasma membrane

doi: 10.64898/2026.04.10.717620

Figure Lengend Snippet: ( A ) Single-step (MOI 5) replication curve of wildtype (WT) and ΔpUL56 HSV-1 in day 14 i3Neurones. Mean ± SD for three independent experiments is shown. ( B ) Schematic of the QTV workflow using day 14 i3Neurones. Mock samples were harvested at 12 hpi for all analyses, and additionally at 3 and 30 hpi for transcriptomics (RNAseq) using Oxford Nanopore Technology (ONT). ( C ) Changes in i3Neurone protein abundance at 30 hpi with WT HSV-1. Horizontal axis shows average fold change and vertical axis shows significance (two-sided t-test) for three independent experiments. Proteins are coloured by FDR-corrected significance and viral proteins are outlined in pink. ( D ) Changes in i3Neurone transcript abundance at 30 hpi with WT HSV-1. Horizontal axis shows average fold change and vertical axis shows FDR-adjusted significance for three independent experiments. Significantly altered genes (log 2 fold change ≥ 2 and p ≤ 0.05) are blue and viral transcripts are outlined in pink. ( E ) Immunoblot analysis of day 14 i3Neurones at 16 hpi (MOI 10) with HSV-1 strains KOS, S17 and SC16, or Semliki Forest virus (SFV)4. Changes in KIF1A, cFOS and GOPC are HSV-1 specific, whereas abundance of stathmins (STMN2–4) is altered in all infections. Capsid proteins VP5 (HSV) and CP (SFV4) confirm successful infection and GAPDH is a loading control. ( F ) Gene Ontology (GO) analysis of proteins (top, blue) and transcripts (bottom, green) with significantly changed abundance at 30 hpi in HSV-versus mock-infected i3Neurones. Significant GO molecular function terms are shown as bubbles sized by magnitude of enrichment, with significance (FDR-adjusted p-value) plotted on the horizontal axis and arrows indicating whether the term was enriched amongst the up- or down-regulated gene products. ( G ) Changes in protein (horizontal) versus transcript (vertical) abundance in mock-versus HSV-infected i3Neurones at 30 hpi. Cellular and viral gene products are grey and pink, respectively, with selected cellular gene products highlighted (black). Potential targets of HSV-1 directed proteasomal degradation (larger fold change in protein vs transcript abundance) are to the left of the dotted red line. (H) Normalised abundance traces of selected proteins (top) and transcripts (bottom) across the time course of infection with WT (pink) or ΔpUL56 (blue) HSV-1. Mock-infected samples (M) are shown as 0 hpi. ( I ) Cellular protein abundance changes in day 14 i3Neurones infected (MOI 5) with WT versus ΔpUL56 i3Neurones. Data are plotted as in ( C ), with horizontal axis showing average mock-corrected fold change for three independent experiments.

Article Snippet: Primary and secondary antibody incubations were performed in TBS supplemented with 0.1% TWEEN-20 and 5% (w/v) skim milk powder using the following antibodies: HSV-1 VP5, ( ); SV4 CP, kindly provided by Andres Merits ( ); KIF1A, BD Transduction Laboratories 612094; cFOS, Cell Signalling Technologies 2250T; GOPC, Abcam Ab133472; STMN2, Novus Biologicals NBP1-49461; STMN3, ProteinTech 11311-1-AP; STMN4, ProteinTech 12027-1-AP; GAPDH, GeneTex GTX28245; HSV-1 pUL56, ( ); HA, Cell Signalling Technologies C29F4; Anti-rabbit 800, LI-COR 926-32213; Anti-rabbit 680, LI-COR 926-68023; Anti-mouse 800, LI-COR 926-32210; Anti-mouse 680, LI-COR 926-68020.

Techniques: Transcriptomics, RNA sequencing, Quantitative Proteomics, Western Blot, Virus, Infection, Control

( A ) Diagram of Mɸ-sensory neuron co-culture paradigm. Made in BioRender. ( B,C ) Representative images of WT DRGs cultured alone (DRG only) or with stimulated WT ( B ) or Sarm1-/- ( C ) Mɸ for 24 hours (mCSF, IL-4, or LPS). Scale bar = 250µm. ( D-F ) Quantification of DRG longest neurite length ( D ), total neurite length ( E ), or number of branch points per neuron of DRGs ( F ) in B , C . Error bars = SEM (N=≥90 neurons with WT Mɸ; ≥ 88 neurons with Sarm1-/- Mɸ ( E ) ≥93 neurons with WT Mɸ; ≥120 neurons with Sarm1-/- Mɸ ( F )≥63 neurons with WT Mɸs; ≥135 neurons with Sarm1-/- Mɸ from 3 independent experiments for WT Mɸ and 2 independent experiments for Sarm1-/- Mɸ. *p<0.05; **p<0.01; ****p<0.0001 by Kruskal-Wallis test with Dunn’s correction for multiple comparisons. ( G ) Representative images of WT or Sarm1-/- Mɸ injected into Sarm1-/- sciatic nerves. Images are 3 days after crush + injection. Mɸ are identified with F4/80 (green), and regenerating axons with SCG10 (Magenta). Arrows indicate regenerating axon tips. ( H,I ) Quantification of SCG10 expression following injection of Mɸ into Sarm1-/- ( H ) or WT ( I ) nerves. N=1-3 biological replicates. Expression was normalized to the injury site and represented as a fold change to the PBS control (black dashed line). Error bars = SEM.

Journal: bioRxiv

Article Title: SARM1 is required for macrophage immunophenotype switching that is essential for nerve repair

doi: 10.64898/2026.04.07.716973

Figure Lengend Snippet: ( A ) Diagram of Mɸ-sensory neuron co-culture paradigm. Made in BioRender. ( B,C ) Representative images of WT DRGs cultured alone (DRG only) or with stimulated WT ( B ) or Sarm1-/- ( C ) Mɸ for 24 hours (mCSF, IL-4, or LPS). Scale bar = 250µm. ( D-F ) Quantification of DRG longest neurite length ( D ), total neurite length ( E ), or number of branch points per neuron of DRGs ( F ) in B , C . Error bars = SEM (N=≥90 neurons with WT Mɸ; ≥ 88 neurons with Sarm1-/- Mɸ ( E ) ≥93 neurons with WT Mɸ; ≥120 neurons with Sarm1-/- Mɸ ( F )≥63 neurons with WT Mɸs; ≥135 neurons with Sarm1-/- Mɸ from 3 independent experiments for WT Mɸ and 2 independent experiments for Sarm1-/- Mɸ. *p<0.05; **p<0.01; ****p<0.0001 by Kruskal-Wallis test with Dunn’s correction for multiple comparisons. ( G ) Representative images of WT or Sarm1-/- Mɸ injected into Sarm1-/- sciatic nerves. Images are 3 days after crush + injection. Mɸ are identified with F4/80 (green), and regenerating axons with SCG10 (Magenta). Arrows indicate regenerating axon tips. ( H,I ) Quantification of SCG10 expression following injection of Mɸ into Sarm1-/- ( H ) or WT ( I ) nerves. N=1-3 biological replicates. Expression was normalized to the injury site and represented as a fold change to the PBS control (black dashed line). Error bars = SEM.

Article Snippet: Primary antibodies diluted in blocking buffer were then added: chicken α-NFH (Aves Labs #NFH 1:100), chicken α-NFM (Aves Labs #NFM 1:100), chicken α-NFL (Aves Labs #NFL 1:100), rabbit α-CD68, (Cell Signaling Technology #E307V 1:500), rabbit α-CD206 (Cell Signaling Technology #E6T5J 1:500), α-SCG10 (Novus Biologicals #NBP1-49461 1:500), α-Myelin Basic Protein (Bio Legend #808401 1:500), α-ATP8A2 (Invitrogen #PA5 −65256 1:500) and/or rat α-F4/80 (Invitrogen #MA1-91124 1:500) and slides were incubated at 4°C overnight.

Techniques: Co-Culture Assay, Cell Culture, Injection, Expressing, Control

( A,B ) Representative images of injury site ( A ) and distal stump ( B ) of sciatic nerves 7 days post SNC. Phosphotidyl serine flippase (Magenta; ATP8A2), Mɸ (Green; F4/80), and myelin (Yellow; MBP). Arrows indicate F4/80 and ATP8A2 positive cells. Scale bar = 50 µm. N = 3 biological replicates. ( C ) Quantification of images in ( A,B ). ATPA82 and MBP were normalized to an uninjured WT nerve. F4/80 signal was measured as intensity/area. N=2-3 biological replicates. Data is mean +/- SEM. *p<0.05 by two-way ANOVA with Dunnett correction for multiple comparisons. ( D ) Representative images of regenerating sensory axons (SCG10; Magenta) at 7d post SNC. N=3 biological replicates. Scale = 500 µm. ( E ) Quantification of relative SCG10 intensity from ( D ) normalized to injury site. Symbols indicate mean and shaded areas indicate SEM. N= 3 biological replicates. ( F-I ) Behavior analyses from BlackBox at 10 timepoints post unilateral SNC. Data in F-H are represented as mean +/- SEM. ( F ) Walking distance recorded in pixels. ( G ) Toe spread ratio of injured hindlimb to uninjured hindlimb. ( H ) Time spent rearing over 20 minutes recorded in seconds. ( I ) Weight bearing ratio of injured to uninjured hind paw. 1 indicates the most pressure recorded. *p<0.05; **p<0.01; ***p<0.005; ****p<0.0001 by two-way ANOVA with Dunnett correction for multiple comparisons. Biological replicates (WT = 10; mac-cKO = 13; neu-cKO =11; Sarm1-/- = 12)

Journal: bioRxiv

Article Title: SARM1 is required for macrophage immunophenotype switching that is essential for nerve repair

doi: 10.64898/2026.04.07.716973

Figure Lengend Snippet: ( A,B ) Representative images of injury site ( A ) and distal stump ( B ) of sciatic nerves 7 days post SNC. Phosphotidyl serine flippase (Magenta; ATP8A2), Mɸ (Green; F4/80), and myelin (Yellow; MBP). Arrows indicate F4/80 and ATP8A2 positive cells. Scale bar = 50 µm. N = 3 biological replicates. ( C ) Quantification of images in ( A,B ). ATPA82 and MBP were normalized to an uninjured WT nerve. F4/80 signal was measured as intensity/area. N=2-3 biological replicates. Data is mean +/- SEM. *p<0.05 by two-way ANOVA with Dunnett correction for multiple comparisons. ( D ) Representative images of regenerating sensory axons (SCG10; Magenta) at 7d post SNC. N=3 biological replicates. Scale = 500 µm. ( E ) Quantification of relative SCG10 intensity from ( D ) normalized to injury site. Symbols indicate mean and shaded areas indicate SEM. N= 3 biological replicates. ( F-I ) Behavior analyses from BlackBox at 10 timepoints post unilateral SNC. Data in F-H are represented as mean +/- SEM. ( F ) Walking distance recorded in pixels. ( G ) Toe spread ratio of injured hindlimb to uninjured hindlimb. ( H ) Time spent rearing over 20 minutes recorded in seconds. ( I ) Weight bearing ratio of injured to uninjured hind paw. 1 indicates the most pressure recorded. *p<0.05; **p<0.01; ***p<0.005; ****p<0.0001 by two-way ANOVA with Dunnett correction for multiple comparisons. Biological replicates (WT = 10; mac-cKO = 13; neu-cKO =11; Sarm1-/- = 12)

Techniques:

Journal: bioRxiv

Article Title: Stathmin-2 Mediates Paracrine Hormone Regulation of Glucagon Through Lysosomal Trafficking in αTC1-6 cells

doi: 10.64898/2026.04.02.715646

Figure Lengend Snippet: A) Images show co-localized immunofluorescence signals for glucagon and Stmn2 (top row), glucagon and the lysosomal marker LAMP1 (middle row) and glucagon and the secretory granule membrane docking protein syntaxin-1A (bottom row). Insets show magnified areas outlined in green. Yellow arrowheads indicate the spatial localization of immunofluorescence signals in peripheral and intracellular regions. B) Plot profile analyses of colocalized immunofluorescence signals in the intracellular or peripheral regions in response to vehicle (open circle), 1 nM insulin+25 μM GABA (open squares), or 400 nM SST (x). Bars represent the averaged colocalized fluorescence intensities ± SEM (n=3) and symbols represent measurements from individual cells. Comparisons were made between and within cellular regions using a two-way ANOVA, followed by a post-hoc test. ***p<0.001, ****p<0.0001.

Article Snippet: Stmn2-GFP was obtained as the Stmn2 mouse tagged ORF clone (OriGene, cat#NM_025285) and pcDNA3-eGFP was used as the vector control.

Techniques: Immunofluorescence, Marker, Membrane, Fluorescence

Transfected cells were immunostained using primary antibodies against Stmn2 (green) and glucagon (red). a) Cells transfected with GFP alone show co-localized signals mainly at the cell periphery (yellow arrowheads). b) In Stmn2-KD cells, there is diminished Stmn2 immunofluorescence with glucagon localized largely to the periphery (yellow arrowheads). c) After Stmn2 OE, there is increased Stmn2 fluorescence intensity colocalizing strongly with glucagon in the intracellular region (yellow arrowheads). d) Changes in integrated Stmn2 fluorescence intensity in the Stmn2-KD and OE compared to the control (GFP-alone), normalized to endogenous Stmn2. Values were expressed as average integrated fluorescence intensity ±SEM (n=6) and compared among groups using a one-way ANOVA, followed by a post-hoc test. **p<0.01, ****p<0.0001. e) Glucagon distribution under control conditions (dark grey bars), and in response to Stmn2-KD (black bars) or OE (light grey bars) with values expressed as average glucagon fluorescence intensity ±SEM (n=6), compared among groups and cellular regions using a two-way ANOVA, followed by a post-hoc test. **p<0.01, ****p<0.0001.

Journal: bioRxiv

Article Title: Stathmin-2 Mediates Paracrine Hormone Regulation of Glucagon Through Lysosomal Trafficking in αTC1-6 cells

doi: 10.64898/2026.04.02.715646

Figure Lengend Snippet: Transfected cells were immunostained using primary antibodies against Stmn2 (green) and glucagon (red). a) Cells transfected with GFP alone show co-localized signals mainly at the cell periphery (yellow arrowheads). b) In Stmn2-KD cells, there is diminished Stmn2 immunofluorescence with glucagon localized largely to the periphery (yellow arrowheads). c) After Stmn2 OE, there is increased Stmn2 fluorescence intensity colocalizing strongly with glucagon in the intracellular region (yellow arrowheads). d) Changes in integrated Stmn2 fluorescence intensity in the Stmn2-KD and OE compared to the control (GFP-alone), normalized to endogenous Stmn2. Values were expressed as average integrated fluorescence intensity ±SEM (n=6) and compared among groups using a one-way ANOVA, followed by a post-hoc test. **p<0.01, ****p<0.0001. e) Glucagon distribution under control conditions (dark grey bars), and in response to Stmn2-KD (black bars) or OE (light grey bars) with values expressed as average glucagon fluorescence intensity ±SEM (n=6), compared among groups and cellular regions using a two-way ANOVA, followed by a post-hoc test. **p<0.01, ****p<0.0001.

Article Snippet: Stmn2-GFP was obtained as the Stmn2 mouse tagged ORF clone (OriGene, cat#NM_025285) and pcDNA3-eGFP was used as the vector control.

Techniques: Transfection, Immunofluorescence, Fluorescence, Control

Transfected cells were treated with 1 nM insulin for 24 hours, then immunostained using primary antibodies against Stmn2 and glucagon. a) Cells transfected with GFP vector and treated with 1 nM insulin showed Stmn2 (green) and glucagon (red) redistributing intracellularly. b) The Stmn2-KD model diminished Stmn2 fluorescence and resulted in glucagon in the periphery, even after 1 nM insulin treatment. c) The Stmn2-OE model increased Stmn2 fluorescence intensity that colocalized strongly with glucagon in the intracellular region after 1 nM insulin treatment. d) Quantification of glucagon distribution in response to Stmn2-KD and OE with values expressed as average glucagon fluorescence intensity ±SEM (n=6), compared among groups and cellular regions using a two-way ANOVA, followed by a post-hoc test. ****p<0.0001.

Journal: bioRxiv

Article Title: Stathmin-2 Mediates Paracrine Hormone Regulation of Glucagon Through Lysosomal Trafficking in αTC1-6 cells

doi: 10.64898/2026.04.02.715646

Figure Lengend Snippet: Transfected cells were treated with 1 nM insulin for 24 hours, then immunostained using primary antibodies against Stmn2 and glucagon. a) Cells transfected with GFP vector and treated with 1 nM insulin showed Stmn2 (green) and glucagon (red) redistributing intracellularly. b) The Stmn2-KD model diminished Stmn2 fluorescence and resulted in glucagon in the periphery, even after 1 nM insulin treatment. c) The Stmn2-OE model increased Stmn2 fluorescence intensity that colocalized strongly with glucagon in the intracellular region after 1 nM insulin treatment. d) Quantification of glucagon distribution in response to Stmn2-KD and OE with values expressed as average glucagon fluorescence intensity ±SEM (n=6), compared among groups and cellular regions using a two-way ANOVA, followed by a post-hoc test. ****p<0.0001.

Article Snippet: Stmn2-GFP was obtained as the Stmn2 mouse tagged ORF clone (OriGene, cat#NM_025285) and pcDNA3-eGFP was used as the vector control.

Techniques: Transfection, Plasmid Preparation, Fluorescence

Transfected cells were treated with 400 nM somatostatin for 24 hours. Cells were then immunostained using primary antibodies against Stmn2 (green) and glucagon (red). a) Cells transfected with GFP vector and treated with 400 nM somatostatin resulted in Stmn2 and glucagon distributing mostly in the intracellular region (yellow arrowheads). b) The Stmn2-KD model diminished Stmn2 fluorescence intensity, and glucagon was present in the periphery after somatostatin treatment. c) The Stmn2-OE model increased Stmn2 fluorescence intensity while colocalizing strongly with glucagon in the intracellular region after somatostatin treatment. d) Glucagon distribution in response to Stmn2-KD (red bars) and OE (green bars) with values expressed as average glucagon fluorescence intensity ±SEM (n=6) and compared among groups and cellular regions using a two-way ANOVA, followed by a post-hoc test. ****p<0.0001.

Journal: bioRxiv

Article Title: Stathmin-2 Mediates Paracrine Hormone Regulation of Glucagon Through Lysosomal Trafficking in αTC1-6 cells

doi: 10.64898/2026.04.02.715646

Figure Lengend Snippet: Transfected cells were treated with 400 nM somatostatin for 24 hours. Cells were then immunostained using primary antibodies against Stmn2 (green) and glucagon (red). a) Cells transfected with GFP vector and treated with 400 nM somatostatin resulted in Stmn2 and glucagon distributing mostly in the intracellular region (yellow arrowheads). b) The Stmn2-KD model diminished Stmn2 fluorescence intensity, and glucagon was present in the periphery after somatostatin treatment. c) The Stmn2-OE model increased Stmn2 fluorescence intensity while colocalizing strongly with glucagon in the intracellular region after somatostatin treatment. d) Glucagon distribution in response to Stmn2-KD (red bars) and OE (green bars) with values expressed as average glucagon fluorescence intensity ±SEM (n=6) and compared among groups and cellular regions using a two-way ANOVA, followed by a post-hoc test. ****p<0.0001.

Article Snippet: Stmn2-GFP was obtained as the Stmn2 mouse tagged ORF clone (OriGene, cat#NM_025285) and pcDNA3-eGFP was used as the vector control.

Techniques: Transfection, Plasmid Preparation, Fluorescence

Cells (n=3) were co-transfected with LAMP1-RFP and GFP vector or Stmn2-GFP, or with scrambled siRNA or siRNA against stathmin-2 (Stmn2-KD) and live images were captured 24 hours post-transfection. a) LAMP1-RFP is present in the cell periphery and the intracellular region (yellow arrowheads) after co-transfection with GFP alone as a negative control (upper panel). After co-transfection with Stmn2-GFP, (lower panel), LAMP1-RFP appears exclusively in the intracellular region (yellow arrowheads). b) LAMP1-RFP is present in the cell periphery and the intracellular region (yellow arrowheads) after co-transfection with scrambled siRNA sequences as a negative control for Stmn2-KD (upper panel). Transfection with Stmn2 siRNAs (KD) resulted in LAMP1-RFP exclusively in the cell periphery (yellow arrowheads) (lower panel). c) Transcription factor EB (TFEB) is not translocated to the nucleus upon overexpression of Stmn2-GFP. Immunofluorescence images of fixed cells show the subcellular distribution of TFEB, GFP alone (upper panel), Stmn2-GFP (lower panel) and cell nuclei (DAPI). Box plots show the ratio of nuclear to cytoplasmic TFEB immunofluorescence. Values were expressed as the average nuclear/cytoplasmic TFEB intensity ±SEM (n=4). Data points in colour represent the average ratio of 8-16 cells per coverslip; black points represent ratios from individual cells. d) Stmn2 regulates the lysosomal transport protein Arl8. Immunofluorescence images of fixed cells show the presence of Arl8 (orange) in cells transfected with scrambled siRNA or siRNA against Stmn2. Quantification of fluorescence (left) shows that knockdown of Stmn2 (Stmn2-KD) significantly increased the fluorescence intensity of Arl8. Values are means ±SEM (n=6). Data points in colour represent the average fluorescence intensities in 8-16 cells per coverslip; black points represent values from individual cells.

Journal: bioRxiv

Article Title: Stathmin-2 Mediates Paracrine Hormone Regulation of Glucagon Through Lysosomal Trafficking in αTC1-6 cells

doi: 10.64898/2026.04.02.715646

Figure Lengend Snippet: Cells (n=3) were co-transfected with LAMP1-RFP and GFP vector or Stmn2-GFP, or with scrambled siRNA or siRNA against stathmin-2 (Stmn2-KD) and live images were captured 24 hours post-transfection. a) LAMP1-RFP is present in the cell periphery and the intracellular region (yellow arrowheads) after co-transfection with GFP alone as a negative control (upper panel). After co-transfection with Stmn2-GFP, (lower panel), LAMP1-RFP appears exclusively in the intracellular region (yellow arrowheads). b) LAMP1-RFP is present in the cell periphery and the intracellular region (yellow arrowheads) after co-transfection with scrambled siRNA sequences as a negative control for Stmn2-KD (upper panel). Transfection with Stmn2 siRNAs (KD) resulted in LAMP1-RFP exclusively in the cell periphery (yellow arrowheads) (lower panel). c) Transcription factor EB (TFEB) is not translocated to the nucleus upon overexpression of Stmn2-GFP. Immunofluorescence images of fixed cells show the subcellular distribution of TFEB, GFP alone (upper panel), Stmn2-GFP (lower panel) and cell nuclei (DAPI). Box plots show the ratio of nuclear to cytoplasmic TFEB immunofluorescence. Values were expressed as the average nuclear/cytoplasmic TFEB intensity ±SEM (n=4). Data points in colour represent the average ratio of 8-16 cells per coverslip; black points represent ratios from individual cells. d) Stmn2 regulates the lysosomal transport protein Arl8. Immunofluorescence images of fixed cells show the presence of Arl8 (orange) in cells transfected with scrambled siRNA or siRNA against Stmn2. Quantification of fluorescence (left) shows that knockdown of Stmn2 (Stmn2-KD) significantly increased the fluorescence intensity of Arl8. Values are means ±SEM (n=6). Data points in colour represent the average fluorescence intensities in 8-16 cells per coverslip; black points represent values from individual cells.

Article Snippet: Stmn2-GFP was obtained as the Stmn2 mouse tagged ORF clone (OriGene, cat#NM_025285) and pcDNA3-eGFP was used as the vector control.

Techniques: Transfection, Plasmid Preparation, Cotransfection, Negative Control, Over Expression, Immunofluorescence, Fluorescence, Knockdown

Live images of αTC1-6 cells transfected with LAMP1-RFP (n=3) were captured in the same cell before, during, and five minutes after treatment with 1 nM insulin. a) LAMP1-RFP redistributed intracellularly (yellow arrowheads) in response to 1 nM insulin treatment in control cells transfected with scrambled siRNA. b) LAMP1-RFP distribution was not changed after 1 nM insulin treatment after siRNA-mediated knockdown of Stmn2 (Stmn2-KD) (yellow arrowheads). Graphs show the distribution of LAMP1-RFP fluorescence intensities in the intracellular and peripheral regions before (pre-INS) and after (post-INS) treatment with 1 nM insulin. Values are means ±SEM (n=3). * p<0.05

Journal: bioRxiv

Article Title: Stathmin-2 Mediates Paracrine Hormone Regulation of Glucagon Through Lysosomal Trafficking in αTC1-6 cells

doi: 10.64898/2026.04.02.715646

Figure Lengend Snippet: Live images of αTC1-6 cells transfected with LAMP1-RFP (n=3) were captured in the same cell before, during, and five minutes after treatment with 1 nM insulin. a) LAMP1-RFP redistributed intracellularly (yellow arrowheads) in response to 1 nM insulin treatment in control cells transfected with scrambled siRNA. b) LAMP1-RFP distribution was not changed after 1 nM insulin treatment after siRNA-mediated knockdown of Stmn2 (Stmn2-KD) (yellow arrowheads). Graphs show the distribution of LAMP1-RFP fluorescence intensities in the intracellular and peripheral regions before (pre-INS) and after (post-INS) treatment with 1 nM insulin. Values are means ±SEM (n=3). * p<0.05

Article Snippet: Stmn2-GFP was obtained as the Stmn2 mouse tagged ORF clone (OriGene, cat#NM_025285) and pcDNA3-eGFP was used as the vector control.

Techniques: Transfection, Control, Knockdown, Fluorescence

αTC1-6 cells (n=3) were transfected overnight. Live images were captured in the same cell before, during, and five minutes after treatment with 400 nM somatostatin. a) LAMP1-RFP redistributed intracellularly (yellow arrowheads) in response to 400 nM somatostatin treatment in control cells transfected with scrambled siRNA. b) LAMP1-RFP distribution was not changed after 400 nM somatostatin treatment after siRNA-mediated knockdown of Stmn2 (Stmn2-KD) (yellow arrowheads). Graphs show means ±SEM (n=3). * p<0.05

Journal: bioRxiv

Article Title: Stathmin-2 Mediates Paracrine Hormone Regulation of Glucagon Through Lysosomal Trafficking in αTC1-6 cells

doi: 10.64898/2026.04.02.715646

Figure Lengend Snippet: αTC1-6 cells (n=3) were transfected overnight. Live images were captured in the same cell before, during, and five minutes after treatment with 400 nM somatostatin. a) LAMP1-RFP redistributed intracellularly (yellow arrowheads) in response to 400 nM somatostatin treatment in control cells transfected with scrambled siRNA. b) LAMP1-RFP distribution was not changed after 400 nM somatostatin treatment after siRNA-mediated knockdown of Stmn2 (Stmn2-KD) (yellow arrowheads). Graphs show means ±SEM (n=3). * p<0.05

Article Snippet: Stmn2-GFP was obtained as the Stmn2 mouse tagged ORF clone (OriGene, cat#NM_025285) and pcDNA3-eGFP was used as the vector control.

Techniques: Transfection, Control, Knockdown

Journal: bioRxiv

Article Title: Stathmin-2 Mediates Paracrine Hormone Regulation of Glucagon Through Lysosomal Trafficking in αTC1-6 cells

doi: 10.64898/2026.04.02.715646

Article Snippet: Stmn2-GFP was obtained as the Stmn2 mouse tagged ORF clone (OriGene, cat#NM_025285) and pcDNA3-eGFP was used as the vector control.

Techniques: Transfection, Plasmid Preparation, Cotransfection, Negative Control, Over Expression, Immunofluorescence, Fluorescence, Knockdown

Review

stathmin 2 stmn2 (Novus Biologicals)

Structured Review

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