plexina1  (Alomone Labs)


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    Structured Review

    Alomone Labs plexina1
    Dynasore blocks internalization of the Sema3A binding receptor (A) Representative images of COS7 cells that were grown on glass dishes for 2DIV and then treated with <t>FITC-PlexinA1</t> antibody with and without Dynasore. The Plexin A1-FITC antibody remained on the cell surface of cells that were treated with the dynamin-dependent endocytosis blocker compared with the untreated group.
    Plexina1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/plexina1/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    plexina1 - by Bioz Stars, 2022-12
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    Images

    1) Product Images from "Sema3A Facilitates a Retrograde Death Signal via CRMP4-Dynein Complex Formation in ALS Motor Axons"

    Article Title: Sema3A Facilitates a Retrograde Death Signal via CRMP4-Dynein Complex Formation in ALS Motor Axons

    Journal: bioRxiv

    doi: 10.1101/774737

    Dynasore blocks internalization of the Sema3A binding receptor (A) Representative images of COS7 cells that were grown on glass dishes for 2DIV and then treated with FITC-PlexinA1 antibody with and without Dynasore. The Plexin A1-FITC antibody remained on the cell surface of cells that were treated with the dynamin-dependent endocytosis blocker compared with the untreated group.
    Figure Legend Snippet: Dynasore blocks internalization of the Sema3A binding receptor (A) Representative images of COS7 cells that were grown on glass dishes for 2DIV and then treated with FITC-PlexinA1 antibody with and without Dynasore. The Plexin A1-FITC antibody remained on the cell surface of cells that were treated with the dynamin-dependent endocytosis blocker compared with the untreated group.

    Techniques Used: Binding Assay

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    Alomone Labs anti plexin a1 extracellular antibody
    Possible <t>Sema6d-Plxna1</t> repellent interactions during optic cup morphogenesis. A , B , EGFP+ eye vesicles from 18-ss wild-type Tg(tfec:EGFP) embryos were explanted and cultured in control media ( A–A’’ ) or in the presence of a soluble Sema6d protein (Sema6d-Fc; B–B’’ ). A’’ , B’’ are magnified views of the boxed areas in A’ , B’ . C , Quantitation of the average number of EGFP+ RPE cells that left the explant in the presence or absence of Sema6d-Fc ( N = 3; n = 8–9 explants/condition each from a separate embryo, error bars are SD; unpaired t test, df = 16). D , Percent of GFP+ RPE coverage over the explanted Tg(tfec:EGFP) optic cup. Eye explants cultured in vitro develop RPE that covers the extent of the explant, whereas those cultured in the presence of soluble Semd6d fragment do not ( N = 3; n = 8–9 explants/condition, each from a separate embryo, error bars are SD; one-way ANOVA, Dunnett’s multiple comparisons test, df = 24). E , Schematic of eye explant culture experiments. F–I , Lateral views of vax2 whole-mount ISH at 24 hpf. Losing Sema6d or inhibition of c-Abl with dasatinib disrupts temporal eye morphogenesis (asterisks). J , Quantitation of optic cup morphogenesis defects by representing the ratio of the width of the temporal versus nasal eye ( N = 3; n = 14–18 embryos/condition, error bars are SD; one-way ANOVA, Dunnett’s multiple comparisons test, df = 59). K , L , Immunolabeling of cryostat sections through the eye vesicle of 18-hpf wild-type ( K ) and sema6d mutant ( L ) embryos for the phosphorylated form of c-Abl ( N = 2 independent experiments). Dotted yellow lines indicate the separation between the neural retina and the RPE. Yellow arrowheads point to labeling of temporal eye vesicle in wild-type, with this label largely absent in mutants. M , Simple repulsion model. Our data support the possibility that Plxna1a from RPE cells activates Sema6d reverse signaling in neural retinal progenitors to promote movement of the cells of the inner eye vesicle around the distal rim of the optic cup. The possibility that Sema6d forward signals to Plxna1a-expressing RPE cells appears less likely. N , Repulsion across the ventricle model. Progenitor RPE cells interact with neural retina cells to allow leaflets to slide over each other during optic cup morphogenesis. Our data support the idea that Sema6d reverse signaling is the main mode involved. O , De-adhesion from ECM model. Progenitor RPE cells interact with neural retina cells to prevent over-adhesion to the ECM. Scale bars: 50 μm ( A , F ).
    Anti Plexin A1 Extracellular Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti plexin a1 extracellular antibody/product/Alomone Labs
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    Alomone Labs plexina1 1
    Possible <t>Sema6d-Plxna1</t> repellent interactions during optic cup morphogenesis. A , B , EGFP+ eye vesicles from 18-ss wild-type Tg(tfec:EGFP) embryos were explanted and cultured in control media ( A–A’’ ) or in the presence of a soluble Sema6d protein (Sema6d-Fc; B–B’’ ). A’’ , B’’ are magnified views of the boxed areas in A’ , B’ . C , Quantitation of the average number of EGFP+ RPE cells that left the explant in the presence or absence of Sema6d-Fc ( N = 3; n = 8–9 explants/condition each from a separate embryo, error bars are SD; unpaired t test, df = 16). D , Percent of GFP+ RPE coverage over the explanted Tg(tfec:EGFP) optic cup. Eye explants cultured in vitro develop RPE that covers the extent of the explant, whereas those cultured in the presence of soluble Semd6d fragment do not ( N = 3; n = 8–9 explants/condition, each from a separate embryo, error bars are SD; one-way ANOVA, Dunnett’s multiple comparisons test, df = 24). E , Schematic of eye explant culture experiments. F–I , Lateral views of vax2 whole-mount ISH at 24 hpf. Losing Sema6d or inhibition of c-Abl with dasatinib disrupts temporal eye morphogenesis (asterisks). J , Quantitation of optic cup morphogenesis defects by representing the ratio of the width of the temporal versus nasal eye ( N = 3; n = 14–18 embryos/condition, error bars are SD; one-way ANOVA, Dunnett’s multiple comparisons test, df = 59). K , L , Immunolabeling of cryostat sections through the eye vesicle of 18-hpf wild-type ( K ) and sema6d mutant ( L ) embryos for the phosphorylated form of c-Abl ( N = 2 independent experiments). Dotted yellow lines indicate the separation between the neural retina and the RPE. Yellow arrowheads point to labeling of temporal eye vesicle in wild-type, with this label largely absent in mutants. M , Simple repulsion model. Our data support the possibility that Plxna1a from RPE cells activates Sema6d reverse signaling in neural retinal progenitors to promote movement of the cells of the inner eye vesicle around the distal rim of the optic cup. The possibility that Sema6d forward signals to Plxna1a-expressing RPE cells appears less likely. N , Repulsion across the ventricle model. Progenitor RPE cells interact with neural retina cells to allow leaflets to slide over each other during optic cup morphogenesis. Our data support the idea that Sema6d reverse signaling is the main mode involved. O , De-adhesion from ECM model. Progenitor RPE cells interact with neural retina cells to prevent over-adhesion to the ECM. Scale bars: 50 μm ( A , F ).
    Plexina1 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/plexina1 1/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    plexina1 1 - by Bioz Stars, 2022-12
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    Image Search Results


    Possible Sema6d-Plxna1 repellent interactions during optic cup morphogenesis. A , B , EGFP+ eye vesicles from 18-ss wild-type Tg(tfec:EGFP) embryos were explanted and cultured in control media ( A–A’’ ) or in the presence of a soluble Sema6d protein (Sema6d-Fc; B–B’’ ). A’’ , B’’ are magnified views of the boxed areas in A’ , B’ . C , Quantitation of the average number of EGFP+ RPE cells that left the explant in the presence or absence of Sema6d-Fc ( N = 3; n = 8–9 explants/condition each from a separate embryo, error bars are SD; unpaired t test, df = 16). D , Percent of GFP+ RPE coverage over the explanted Tg(tfec:EGFP) optic cup. Eye explants cultured in vitro develop RPE that covers the extent of the explant, whereas those cultured in the presence of soluble Semd6d fragment do not ( N = 3; n = 8–9 explants/condition, each from a separate embryo, error bars are SD; one-way ANOVA, Dunnett’s multiple comparisons test, df = 24). E , Schematic of eye explant culture experiments. F–I , Lateral views of vax2 whole-mount ISH at 24 hpf. Losing Sema6d or inhibition of c-Abl with dasatinib disrupts temporal eye morphogenesis (asterisks). J , Quantitation of optic cup morphogenesis defects by representing the ratio of the width of the temporal versus nasal eye ( N = 3; n = 14–18 embryos/condition, error bars are SD; one-way ANOVA, Dunnett’s multiple comparisons test, df = 59). K , L , Immunolabeling of cryostat sections through the eye vesicle of 18-hpf wild-type ( K ) and sema6d mutant ( L ) embryos for the phosphorylated form of c-Abl ( N = 2 independent experiments). Dotted yellow lines indicate the separation between the neural retina and the RPE. Yellow arrowheads point to labeling of temporal eye vesicle in wild-type, with this label largely absent in mutants. M , Simple repulsion model. Our data support the possibility that Plxna1a from RPE cells activates Sema6d reverse signaling in neural retinal progenitors to promote movement of the cells of the inner eye vesicle around the distal rim of the optic cup. The possibility that Sema6d forward signals to Plxna1a-expressing RPE cells appears less likely. N , Repulsion across the ventricle model. Progenitor RPE cells interact with neural retina cells to allow leaflets to slide over each other during optic cup morphogenesis. Our data support the idea that Sema6d reverse signaling is the main mode involved. O , De-adhesion from ECM model. Progenitor RPE cells interact with neural retina cells to prevent over-adhesion to the ECM. Scale bars: 50 μm ( A , F ).

    Journal: eNeuro

    Article Title: Retinal Pigment Epithelium and Neural Retinal Progenitors Interact via Semaphorin 6D to Facilitate Optic Cup Morphogenesis

    doi: 10.1523/ENEURO.0053-21.2021

    Figure Lengend Snippet: Possible Sema6d-Plxna1 repellent interactions during optic cup morphogenesis. A , B , EGFP+ eye vesicles from 18-ss wild-type Tg(tfec:EGFP) embryos were explanted and cultured in control media ( A–A’’ ) or in the presence of a soluble Sema6d protein (Sema6d-Fc; B–B’’ ). A’’ , B’’ are magnified views of the boxed areas in A’ , B’ . C , Quantitation of the average number of EGFP+ RPE cells that left the explant in the presence or absence of Sema6d-Fc ( N = 3; n = 8–9 explants/condition each from a separate embryo, error bars are SD; unpaired t test, df = 16). D , Percent of GFP+ RPE coverage over the explanted Tg(tfec:EGFP) optic cup. Eye explants cultured in vitro develop RPE that covers the extent of the explant, whereas those cultured in the presence of soluble Semd6d fragment do not ( N = 3; n = 8–9 explants/condition, each from a separate embryo, error bars are SD; one-way ANOVA, Dunnett’s multiple comparisons test, df = 24). E , Schematic of eye explant culture experiments. F–I , Lateral views of vax2 whole-mount ISH at 24 hpf. Losing Sema6d or inhibition of c-Abl with dasatinib disrupts temporal eye morphogenesis (asterisks). J , Quantitation of optic cup morphogenesis defects by representing the ratio of the width of the temporal versus nasal eye ( N = 3; n = 14–18 embryos/condition, error bars are SD; one-way ANOVA, Dunnett’s multiple comparisons test, df = 59). K , L , Immunolabeling of cryostat sections through the eye vesicle of 18-hpf wild-type ( K ) and sema6d mutant ( L ) embryos for the phosphorylated form of c-Abl ( N = 2 independent experiments). Dotted yellow lines indicate the separation between the neural retina and the RPE. Yellow arrowheads point to labeling of temporal eye vesicle in wild-type, with this label largely absent in mutants. M , Simple repulsion model. Our data support the possibility that Plxna1a from RPE cells activates Sema6d reverse signaling in neural retinal progenitors to promote movement of the cells of the inner eye vesicle around the distal rim of the optic cup. The possibility that Sema6d forward signals to Plxna1a-expressing RPE cells appears less likely. N , Repulsion across the ventricle model. Progenitor RPE cells interact with neural retina cells to allow leaflets to slide over each other during optic cup morphogenesis. Our data support the idea that Sema6d reverse signaling is the main mode involved. O , De-adhesion from ECM model. Progenitor RPE cells interact with neural retina cells to prevent over-adhesion to the ECM. Scale bars: 50 μm ( A , F ).

    Article Snippet: Sections were processed for immunostaining with the following antibodies; a rabbit polyclonal against the extracellular domain of human PLXNA1 (Alomone, catalog #APR-081, lot #Apr081AN0125), followed by an Alexa Fluor 488 secondary antibody (Invitrogen), and c-Abl (phospho-Tyr245; Aviva Systems Biology) at 1:50. c-Abl immunolabeling involved a two-step secondary; unconjugated mouse anti-rabbit at 1:1000 (Jackson) and Alexa Fluor 555 anti-mouse at 1:1000.

    Techniques: Cell Culture, Quantitation Assay, In Vitro, In Situ Hybridization, Inhibition, Immunolabeling, Mutagenesis, Labeling, Expressing

    sema6d and plxna1a are expressed in complementary domains in the early eye vesicle. A , Lateral view of a 16-ss zebrafish embryo shows sema6d transcript in the eye vesicle, and regions of the head and trunk. B , C , Embryos processed for RNA ISH reveal transcript present in the optic vesicle at the 14-ss ( plxna1a ) and 18-ss ( plxna1b ) stage. D–F , Transverse sections (line in A ) through the brain and eye. sema6d transcript is expressed in the ventral (future temporal) domain of the inner eye vesicle leaflet (arrows) and neural retina (outer leaflet), but is absent from the dorsal (future nasal), presumptive RPE progenitor (pRPE) domain (bar; D ). plxna1a mRNA is present in the pRPE domain (bar) and faintly in the dorsal neural retina (asterisk), but absent from the ventral inner and outer eye vesicle leaflet ( E ). plxna1b is expressed in scattered cells of the outer leaflet of the developing optic cup ( F ). G , H , Eye vesicle (viewed dorsally) at the 16 ss processed for whole-mount ISH with antisense riboprobes for plxna1a (arrows in G ) or the RPE marker, pmel1a ( H ). I , Plxna1-like immunoreactivity is present at the 16 ss in the pRPE domain (arrows). J–L , Schematics of the eye vesicle ( J ), the early embryo axes with respect to the eye ( K ), and optic cup morphogenesis ( L ); note that as the eye rotates alongside brain development, early ventral retina tissue (pink) becomes mature temporal tissue. M , Schematic of plxna1a and sema6d mRNA expression in the 16-ss eye vesicle. Scale bars: 300 μm ( A ) and 50 μm ( D ). br: brain, D: dorsal, e: eye, il: inner leaflet, N: nasal, nk: neural keel, nr: neural retina, ol: outer leaflet, os: optic stalk, pRPE: presumptive RPE, RPE: retinal pigment epithelium, T: temporal, V: ventral, ve: ventricle.

    Journal: eNeuro

    Article Title: Retinal Pigment Epithelium and Neural Retinal Progenitors Interact via Semaphorin 6D to Facilitate Optic Cup Morphogenesis

    doi: 10.1523/ENEURO.0053-21.2021

    Figure Lengend Snippet: sema6d and plxna1a are expressed in complementary domains in the early eye vesicle. A , Lateral view of a 16-ss zebrafish embryo shows sema6d transcript in the eye vesicle, and regions of the head and trunk. B , C , Embryos processed for RNA ISH reveal transcript present in the optic vesicle at the 14-ss ( plxna1a ) and 18-ss ( plxna1b ) stage. D–F , Transverse sections (line in A ) through the brain and eye. sema6d transcript is expressed in the ventral (future temporal) domain of the inner eye vesicle leaflet (arrows) and neural retina (outer leaflet), but is absent from the dorsal (future nasal), presumptive RPE progenitor (pRPE) domain (bar; D ). plxna1a mRNA is present in the pRPE domain (bar) and faintly in the dorsal neural retina (asterisk), but absent from the ventral inner and outer eye vesicle leaflet ( E ). plxna1b is expressed in scattered cells of the outer leaflet of the developing optic cup ( F ). G , H , Eye vesicle (viewed dorsally) at the 16 ss processed for whole-mount ISH with antisense riboprobes for plxna1a (arrows in G ) or the RPE marker, pmel1a ( H ). I , Plxna1-like immunoreactivity is present at the 16 ss in the pRPE domain (arrows). J–L , Schematics of the eye vesicle ( J ), the early embryo axes with respect to the eye ( K ), and optic cup morphogenesis ( L ); note that as the eye rotates alongside brain development, early ventral retina tissue (pink) becomes mature temporal tissue. M , Schematic of plxna1a and sema6d mRNA expression in the 16-ss eye vesicle. Scale bars: 300 μm ( A ) and 50 μm ( D ). br: brain, D: dorsal, e: eye, il: inner leaflet, N: nasal, nk: neural keel, nr: neural retina, ol: outer leaflet, os: optic stalk, pRPE: presumptive RPE, RPE: retinal pigment epithelium, T: temporal, V: ventral, ve: ventricle.

    Article Snippet: Sections were processed for immunostaining with the following antibodies; a rabbit polyclonal against the extracellular domain of human PLXNA1 (Alomone, catalog #APR-081, lot #Apr081AN0125), followed by an Alexa Fluor 488 secondary antibody (Invitrogen), and c-Abl (phospho-Tyr245; Aviva Systems Biology) at 1:50. c-Abl immunolabeling involved a two-step secondary; unconjugated mouse anti-rabbit at 1:1000 (Jackson) and Alexa Fluor 555 anti-mouse at 1:1000.

    Techniques: In Situ Hybridization, Marker, Expressing

    Plxna1a loss-of-function recapitulates the temporal eye defects observed in sema6d mutants. A , B , RT-PCR confirming morpholino mis-splicing (outlined in schematic) of plxna1a transcript ( A ), and knock down of plxna1a transcript in CRISPRi-injected embryos ( B ). β-Actin mRNA as loading control. C , D , Normal expansion of the bhlhe40 -expressing RPE progenitor domain at the 14 ss. Mean anteroposterior eye vesicle length ( C ) and percent RPE expansion ( D ; RPE bhlhe40+ domain length/anteroposterior eye vesicle length) are not significantly different in plxna1a morphants as compared with controls [ N = 2, control n = 17, plxna1 MO n = 17; p values are unpaired t tests, df = 33 ( C ), df = 18 ( D ), error bars are SD]. E , F , Tg(vsx1:GFP) expression in the nasal retina. G , H , vax2 mRNA in lateral views of a control ( G ) and a plxna1a morphant ( H ) 24-hpf eye. I , J , Transverse sections of whole-mount foxd1+ RNA ISH of 24-hpf eyes. Early ventral (future temporal) foxd1+ tissue undergoes rim movement into the outer leaflet in control ( I ), but in a plxna1a morphant remains partially in the inner leaflet ( J ; red asterisk and compare bars). Also evident is an open ventricle (arrow in J ) in the morphant. K , The average angle formed by the lateral edges of the vsx1 ( J ) domain to the center of the lens (θ) is similar between controls and plxna1a morphants ( N = 2; control n = 16, plxna1a MO n = 19, p value is unpaired t test, df = 33). L , Ratio of the width of the temporal to nasal (t and n in G ) vax2 whole-mount RNA ISH domain measured in images of lateral eyes (unpaired t test, p

    Journal: eNeuro

    Article Title: Retinal Pigment Epithelium and Neural Retinal Progenitors Interact via Semaphorin 6D to Facilitate Optic Cup Morphogenesis

    doi: 10.1523/ENEURO.0053-21.2021

    Figure Lengend Snippet: Plxna1a loss-of-function recapitulates the temporal eye defects observed in sema6d mutants. A , B , RT-PCR confirming morpholino mis-splicing (outlined in schematic) of plxna1a transcript ( A ), and knock down of plxna1a transcript in CRISPRi-injected embryos ( B ). β-Actin mRNA as loading control. C , D , Normal expansion of the bhlhe40 -expressing RPE progenitor domain at the 14 ss. Mean anteroposterior eye vesicle length ( C ) and percent RPE expansion ( D ; RPE bhlhe40+ domain length/anteroposterior eye vesicle length) are not significantly different in plxna1a morphants as compared with controls [ N = 2, control n = 17, plxna1 MO n = 17; p values are unpaired t tests, df = 33 ( C ), df = 18 ( D ), error bars are SD]. E , F , Tg(vsx1:GFP) expression in the nasal retina. G , H , vax2 mRNA in lateral views of a control ( G ) and a plxna1a morphant ( H ) 24-hpf eye. I , J , Transverse sections of whole-mount foxd1+ RNA ISH of 24-hpf eyes. Early ventral (future temporal) foxd1+ tissue undergoes rim movement into the outer leaflet in control ( I ), but in a plxna1a morphant remains partially in the inner leaflet ( J ; red asterisk and compare bars). Also evident is an open ventricle (arrow in J ) in the morphant. K , The average angle formed by the lateral edges of the vsx1 ( J ) domain to the center of the lens (θ) is similar between controls and plxna1a morphants ( N = 2; control n = 16, plxna1a MO n = 19, p value is unpaired t test, df = 33). L , Ratio of the width of the temporal to nasal (t and n in G ) vax2 whole-mount RNA ISH domain measured in images of lateral eyes (unpaired t test, p

    Article Snippet: Sections were processed for immunostaining with the following antibodies; a rabbit polyclonal against the extracellular domain of human PLXNA1 (Alomone, catalog #APR-081, lot #Apr081AN0125), followed by an Alexa Fluor 488 secondary antibody (Invitrogen), and c-Abl (phospho-Tyr245; Aviva Systems Biology) at 1:50. c-Abl immunolabeling involved a two-step secondary; unconjugated mouse anti-rabbit at 1:1000 (Jackson) and Alexa Fluor 555 anti-mouse at 1:1000.

    Techniques: Reverse Transcription Polymerase Chain Reaction, Injection, Expressing, In Situ Hybridization

    AnkB440 and its interaction with L1CAM are required for F-actin disassembly during GC collapse upon Sema 3A signaling. ( A ) (Western blot analysis of the expression of Cofilin, phospho-cofilin (Ser3) and LIMK1 in the cortex of PND1 control and AnkB440 KO mice. Actin is a loading control. ( B ) Quantification of total levels of cofilin and LIMK1 normalized to actin in cortical lysates from PND1 AnkB440 KO mice relative to their levels in control brains. ( C ) Quantification of levels of phosho-cofilin relative to total cofilin in cortical lysates from PND1 control and AnkB440 KO mice. Data in B and C represent mean ± SEM for three biological replicates per genotype. Unpaired t test. *p

    Journal: bioRxiv

    Article Title: Giant ankyrin-B mediates transduction of axon guidance and collateral branch pruning factor Sema 3A

    doi: 10.1101/2021.05.03.442401

    Figure Lengend Snippet: AnkB440 and its interaction with L1CAM are required for F-actin disassembly during GC collapse upon Sema 3A signaling. ( A ) (Western blot analysis of the expression of Cofilin, phospho-cofilin (Ser3) and LIMK1 in the cortex of PND1 control and AnkB440 KO mice. Actin is a loading control. ( B ) Quantification of total levels of cofilin and LIMK1 normalized to actin in cortical lysates from PND1 AnkB440 KO mice relative to their levels in control brains. ( C ) Quantification of levels of phosho-cofilin relative to total cofilin in cortical lysates from PND1 control and AnkB440 KO mice. Data in B and C represent mean ± SEM for three biological replicates per genotype. Unpaired t test. *p

    Article Snippet: We also used rabbit anti-Plexin A1 (1:200, # APR-081, Alomone), rabbit anti-phospho-Cofilin (Ser3) (1:1,000, #3311) and rabbit anti-LIMK1 (1:1,000, #3842) from Cell Signaling, mouse anti-cofilin (1:1,000, clone 1G6A2, Proteintech), mouse pan anti-actin (1:2,000, clone C4, #MAB1501, Millipore-Sigma), and mouse anti-GluR1 (1:500, clone N355/1, #75-327, NeuroMab).

    Techniques: Western Blot, Expressing, Mouse Assay