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R&D Systems brain derived neurotrophic factor
Identification of BX795 by high content screening of a kinase inhibitor library. a Directed differentiation of Pax6+ (green)/Nestin+ (red) neural precursor cells (NPCs; DIV 0, left) into TUJ1+ (red)/ TH+ (green) neurons (DIV 21, right). The differentiation protocol and timeline of analysis are shown in the drawing in the middle. FG2 and FGF8, fibroblast growth factors 2 and 8; SHH Sonic Hedgehog, AA ascorbic acid, Scale bar represents BDNF <t>brain-derived</t> <t>neurotrophic</t> <t>factor,</t> GDNF glial cell-derived neurotrophic factor (GDNF), cAMP cyclic AMP. Scale bars, 50 μm. b Scatter plot showing the ratio of TH versus TUJ1 fluorescence intensity in duplicate upon treatment with 273 small molecule kinase inhibitors. The dots inside the green square correspond to the 4 hit compounds showing significant increase of TH versus TUJ1 fluorescence ratio as compared to the DMSO controls (blue dots). The red arrow indicates BX795. c Representative images of patient-derived p.A53T-neurons immunolabelled for TH in 384-well plates. Upper micrograph shows control DMSO-treated cells while lower micrograph represents BX795-treated cells. Scale bar represents 150 μm. d Tests of the four hit compounds in a dose-response format. Data are presented as mean ± SEM. (one-way ANOVA, * P
Brain Derived Neurotrophic Factor, supplied by R&D Systems, used in various techniques. Bioz Stars score: 98/100, based on 40 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "High content screening and proteomic analysis identify a kinase inhibitor that rescues pathological phenotypes in a patient-derived model of Parkinson’s disease"

Article Title: High content screening and proteomic analysis identify a kinase inhibitor that rescues pathological phenotypes in a patient-derived model of Parkinson’s disease

Journal: NPJ Parkinson's Disease

doi: 10.1038/s41531-022-00278-y

Identification of BX795 by high content screening of a kinase inhibitor library. a Directed differentiation of Pax6+ (green)/Nestin+ (red) neural precursor cells (NPCs; DIV 0, left) into TUJ1+ (red)/ TH+ (green) neurons (DIV 21, right). The differentiation protocol and timeline of analysis are shown in the drawing in the middle. FG2 and FGF8, fibroblast growth factors 2 and 8; SHH Sonic Hedgehog, AA ascorbic acid, Scale bar represents BDNF brain-derived neurotrophic factor, GDNF glial cell-derived neurotrophic factor (GDNF), cAMP cyclic AMP. Scale bars, 50 μm. b Scatter plot showing the ratio of TH versus TUJ1 fluorescence intensity in duplicate upon treatment with 273 small molecule kinase inhibitors. The dots inside the green square correspond to the 4 hit compounds showing significant increase of TH versus TUJ1 fluorescence ratio as compared to the DMSO controls (blue dots). The red arrow indicates BX795. c Representative images of patient-derived p.A53T-neurons immunolabelled for TH in 384-well plates. Upper micrograph shows control DMSO-treated cells while lower micrograph represents BX795-treated cells. Scale bar represents 150 μm. d Tests of the four hit compounds in a dose-response format. Data are presented as mean ± SEM. (one-way ANOVA, * P
Figure Legend Snippet: Identification of BX795 by high content screening of a kinase inhibitor library. a Directed differentiation of Pax6+ (green)/Nestin+ (red) neural precursor cells (NPCs; DIV 0, left) into TUJ1+ (red)/ TH+ (green) neurons (DIV 21, right). The differentiation protocol and timeline of analysis are shown in the drawing in the middle. FG2 and FGF8, fibroblast growth factors 2 and 8; SHH Sonic Hedgehog, AA ascorbic acid, Scale bar represents BDNF brain-derived neurotrophic factor, GDNF glial cell-derived neurotrophic factor (GDNF), cAMP cyclic AMP. Scale bars, 50 μm. b Scatter plot showing the ratio of TH versus TUJ1 fluorescence intensity in duplicate upon treatment with 273 small molecule kinase inhibitors. The dots inside the green square correspond to the 4 hit compounds showing significant increase of TH versus TUJ1 fluorescence ratio as compared to the DMSO controls (blue dots). The red arrow indicates BX795. c Representative images of patient-derived p.A53T-neurons immunolabelled for TH in 384-well plates. Upper micrograph shows control DMSO-treated cells while lower micrograph represents BX795-treated cells. Scale bar represents 150 μm. d Tests of the four hit compounds in a dose-response format. Data are presented as mean ± SEM. (one-way ANOVA, * P

Techniques Used: High Content Screening, Derivative Assay, Fluorescence

2) Product Images from "Induced pluripotent stem cell-derived motor neurons from amyotrophic lateral sclerosis (ALS) patients carrying different superoxide dismutase 1 mutations recapitulate pathological features of ALS"

Article Title: Induced pluripotent stem cell-derived motor neurons from amyotrophic lateral sclerosis (ALS) patients carrying different superoxide dismutase 1 mutations recapitulate pathological features of ALS

Journal: Chinese Medical Journal

doi: 10.1097/CM9.0000000000001693

Differentiation of human iPS cells into motor neurons. (A) Overview of human iPS cell differentiation into MNs. EB medium (DMEM/F12, containing 2% B27 and 1% N2, supplemented with 1% NEAA, 200 nmol/L dorsomorphin, 10 μmol/L SB-431542), RA retinoic acid, low and high SHH 50-100 ng/mL sonic hedgehog, PO/LAM, neurobasal medium (2% B27 and 1% N2, with 10 ng/mL BDNF and GDNF). (B) The representative image of morphology of EBs at day 6, neural progenitors at day 14, and motor neuron-like cells at day 28 of controls (control cell line:cell line C3) and ALS patients (SOD1-V14M: cell line: L6); scale bar 1.00 mm. (C) Immunostaining of control and patient-specific MN cultures; motor neurons co-express TUJ1/HB9 and TUJ1/ISL1, nuclei are counterstained with DAPI, shown in blue; scale bar = 50 μm. (D) Quantitative analyses of cells co-express positive for TUJ1/HB9. Bars represent average with SEM as error bars. Data for CONT is the average of 4 iPSC lines, for ALS from 4 iPSC lines. No significant differences were found in the ability of iPSC to generate neurons after 28 days of differentiation. (E) Quantitative analyses of cells co-express positive for TUJ1/ISL1. iPS: Induced pluripotent stem; MNs: Mechanisms in motor neurons; EB: Embryoid body; BDNF: Brain-derived neurotrophic factor; GDNF: Glial cell line-derived neurotrophic factor; SEM: Standard error of mean; CONT: Healthy individuals with no history of neurological disease; PO/LAM: Poly-DL-ornithine and laminin; NEAA: Non-essential amino acid; DAPI: 4′, 6-diamidino-2-phenylindole.
Figure Legend Snippet: Differentiation of human iPS cells into motor neurons. (A) Overview of human iPS cell differentiation into MNs. EB medium (DMEM/F12, containing 2% B27 and 1% N2, supplemented with 1% NEAA, 200 nmol/L dorsomorphin, 10 μmol/L SB-431542), RA retinoic acid, low and high SHH 50-100 ng/mL sonic hedgehog, PO/LAM, neurobasal medium (2% B27 and 1% N2, with 10 ng/mL BDNF and GDNF). (B) The representative image of morphology of EBs at day 6, neural progenitors at day 14, and motor neuron-like cells at day 28 of controls (control cell line:cell line C3) and ALS patients (SOD1-V14M: cell line: L6); scale bar 1.00 mm. (C) Immunostaining of control and patient-specific MN cultures; motor neurons co-express TUJ1/HB9 and TUJ1/ISL1, nuclei are counterstained with DAPI, shown in blue; scale bar = 50 μm. (D) Quantitative analyses of cells co-express positive for TUJ1/HB9. Bars represent average with SEM as error bars. Data for CONT is the average of 4 iPSC lines, for ALS from 4 iPSC lines. No significant differences were found in the ability of iPSC to generate neurons after 28 days of differentiation. (E) Quantitative analyses of cells co-express positive for TUJ1/ISL1. iPS: Induced pluripotent stem; MNs: Mechanisms in motor neurons; EB: Embryoid body; BDNF: Brain-derived neurotrophic factor; GDNF: Glial cell line-derived neurotrophic factor; SEM: Standard error of mean; CONT: Healthy individuals with no history of neurological disease; PO/LAM: Poly-DL-ornithine and laminin; NEAA: Non-essential amino acid; DAPI: 4′, 6-diamidino-2-phenylindole.

Techniques Used: Cell Differentiation, Laser Capture Microdissection, Immunostaining, Derivative Assay

3) Product Images from "High Content Screening and Proteomic Analysis Identify a Kinase Inhibitor that rescues pathological phenotypes in a Patient-Derived Model of Parkinson’s Disease"

Article Title: High Content Screening and Proteomic Analysis Identify a Kinase Inhibitor that rescues pathological phenotypes in a Patient-Derived Model of Parkinson’s Disease

Journal: bioRxiv

doi: 10.1101/2020.06.12.148031

Identification of BX795 by high content screening of a kinase inhibitor library a. Directed differentiation of Pax6+ (green)/ Nestin+ (red) neural precursor cells (NPCs; DIV 0, left) into TUJ1+ (red)/ TH+ (green) neurons (DIV 21, right). The differentiation protocol and timeline of analysis are shown in the drawing in the middle.. FG2 and FGF8, fibroblast growth factors 2 and 8; SHH, Sonic Hedgehog; AA, ascorbic acid; Scale bar represents BDNF, brain-derived neurotrophic factor; GDNF, glial cell-derived neurotrophic factor (GDNF); cAMP, cyclic AMP. Scale bars, 50 μm. b. Scatter plot showing the ratio of TH versus TUJ1 fluorescence intensity in duplicate upon treatment with 273 small molecule kinase inhibitors. The dots inside the green square correspond to the 4 hit compounds showing significant increase of TH versus TUJ1 fluorescence ratio as compared to the DMSO controls (blue dots). The red arrow indicates BX795. c. Representative images of patient-derived p.A53T-neurons immunolabelled for TH in 384-well plates. Upper micrograph shows control DMSO-treated cells while lower micrograph represents BX795-treated cells. Scale bar represents 150 μm. d. Tests of the four hit compounds in a dose-response format. Data are presented as mean ± SEM.(one-way ANOVA, *P
Figure Legend Snippet: Identification of BX795 by high content screening of a kinase inhibitor library a. Directed differentiation of Pax6+ (green)/ Nestin+ (red) neural precursor cells (NPCs; DIV 0, left) into TUJ1+ (red)/ TH+ (green) neurons (DIV 21, right). The differentiation protocol and timeline of analysis are shown in the drawing in the middle.. FG2 and FGF8, fibroblast growth factors 2 and 8; SHH, Sonic Hedgehog; AA, ascorbic acid; Scale bar represents BDNF, brain-derived neurotrophic factor; GDNF, glial cell-derived neurotrophic factor (GDNF); cAMP, cyclic AMP. Scale bars, 50 μm. b. Scatter plot showing the ratio of TH versus TUJ1 fluorescence intensity in duplicate upon treatment with 273 small molecule kinase inhibitors. The dots inside the green square correspond to the 4 hit compounds showing significant increase of TH versus TUJ1 fluorescence ratio as compared to the DMSO controls (blue dots). The red arrow indicates BX795. c. Representative images of patient-derived p.A53T-neurons immunolabelled for TH in 384-well plates. Upper micrograph shows control DMSO-treated cells while lower micrograph represents BX795-treated cells. Scale bar represents 150 μm. d. Tests of the four hit compounds in a dose-response format. Data are presented as mean ± SEM.(one-way ANOVA, *P

Techniques Used: High Content Screening, Derivative Assay, Fluorescence

4) Product Images from "Exercise-Induced Elevated BDNF Level Does Not Prevent Cognitive Impairment Due to Acute Exposure to Moderate Hypoxia in Well-Trained Athletes"

Article Title: Exercise-Induced Elevated BDNF Level Does Not Prevent Cognitive Impairment Due to Acute Exposure to Moderate Hypoxia in Well-Trained Athletes

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms21155569

Brain-derived neurotrophic factor (BDNF) serum concentration at rest, during maximal effort (max) and after 1 h recovery of the recovery period in normoxia and hypoxia (3000 m). ** p
Figure Legend Snippet: Brain-derived neurotrophic factor (BDNF) serum concentration at rest, during maximal effort (max) and after 1 h recovery of the recovery period in normoxia and hypoxia (3000 m). ** p

Techniques Used: Derivative Assay, Concentration Assay

5) Product Images from "Neurotrophic Factor-Laden Acellular Chondroitin Sulfate Scaffolds Promote Chronic Functional Recovery After Severe Traumatic Brain Injury"

Article Title: Neurotrophic Factor-Laden Acellular Chondroitin Sulfate Scaffolds Promote Chronic Functional Recovery After Severe Traumatic Brain Injury

Journal: bioRxiv

doi: 10.1101/2020.06.21.116970

eCS implants promote NSC proliferation and neurotrophic factor expression A – Representative tiled images of ipsilesional hemisphere (left coronal sections) of eCS rat brain tissue; scale bar = 1mm. A1-A4 – representative magnification of dashed white square shown in C for DAPI (A1), Sox1 (A2), Ki67(A3) and merged (A4); scale bar is 100 μm; B – Representative tiled images of ipsilesional hemisphere (left coronal sections) of eCS rat brain tissue; scale bar = 1mm. B1-B4 – representative magnification of dashed white square shown in A for DAPI (B1), CS56 (B2), FGF2 (B3) and merged (B4); scale bar is 100 μm; C – Co-localization Sox1+ cells with Ki67+ cells as percentage of Ki67+ cells for each treatment. Kruskal-Wallis, Treatment: p
Figure Legend Snippet: eCS implants promote NSC proliferation and neurotrophic factor expression A – Representative tiled images of ipsilesional hemisphere (left coronal sections) of eCS rat brain tissue; scale bar = 1mm. A1-A4 – representative magnification of dashed white square shown in C for DAPI (A1), Sox1 (A2), Ki67(A3) and merged (A4); scale bar is 100 μm; B – Representative tiled images of ipsilesional hemisphere (left coronal sections) of eCS rat brain tissue; scale bar = 1mm. B1-B4 – representative magnification of dashed white square shown in A for DAPI (B1), CS56 (B2), FGF2 (B3) and merged (B4); scale bar is 100 μm; C – Co-localization Sox1+ cells with Ki67+ cells as percentage of Ki67+ cells for each treatment. Kruskal-Wallis, Treatment: p

Techniques Used: Expressing

6) Product Images from "High Content Screening and Proteomic Analysis Identify the Kinase Inhibitor BX795 as a Potent Neuroprotective Compound in a Patient-Derived Model of Parkinson’s Disease"

Article Title: High Content Screening and Proteomic Analysis Identify the Kinase Inhibitor BX795 as a Potent Neuroprotective Compound in a Patient-Derived Model of Parkinson’s Disease

Journal: bioRxiv

doi: 10.1101/2020.06.12.148031

Identification of BX795 by high content screening of a kinase inhibitor library A. Directed differentiation of Pax6+ (green)/ Nestin+ (red) neural precursor cells (NPCs; DIV 0, left) into TUJ1+ (red)/ TH+ (green) neurons (DIV 21, right). The differentiation protocol and timeline of analysis are shown in the drawing in the middle. The 273 kinase inhibitors were added at DIV 7 and image acquisition was performed at DIV 21. FG2 and FGF8, fibroblast growth factors 2 and 8; SHH, Sonic Hedgehog; AA, ascorbic acid; Scale bar represents BDNF, brain-derived neurotrophic factor; GDNF, glial cell-derived neurotrophic factor (GDNF); cAMP, cyclic AMP. Scale bars, 50 μm. B. Scatter plot showing the ratio of TH versus Tuj1 expression in duplicate upon drug treatment with 273 small kinase molecule inhibitors. The dots inside the green square correspond to the 4 hit compounds show significant increase TH versus Tuj1 expression ratio as compared to the DMSO controls (blue dots). The red arrow indicates BX795. C. Representative images of p.A53T-neurons immunolabelled for TH in 384-well plates. Upper micrograph shows control DMSO-treated cells while lower micrograph represents BX795-treated cells. Scale bar represents 150 μm. D. Tests of the four hit compounds in a dose-response format. Data are presented as mean ± SEM.
Figure Legend Snippet: Identification of BX795 by high content screening of a kinase inhibitor library A. Directed differentiation of Pax6+ (green)/ Nestin+ (red) neural precursor cells (NPCs; DIV 0, left) into TUJ1+ (red)/ TH+ (green) neurons (DIV 21, right). The differentiation protocol and timeline of analysis are shown in the drawing in the middle. The 273 kinase inhibitors were added at DIV 7 and image acquisition was performed at DIV 21. FG2 and FGF8, fibroblast growth factors 2 and 8; SHH, Sonic Hedgehog; AA, ascorbic acid; Scale bar represents BDNF, brain-derived neurotrophic factor; GDNF, glial cell-derived neurotrophic factor (GDNF); cAMP, cyclic AMP. Scale bars, 50 μm. B. Scatter plot showing the ratio of TH versus Tuj1 expression in duplicate upon drug treatment with 273 small kinase molecule inhibitors. The dots inside the green square correspond to the 4 hit compounds show significant increase TH versus Tuj1 expression ratio as compared to the DMSO controls (blue dots). The red arrow indicates BX795. C. Representative images of p.A53T-neurons immunolabelled for TH in 384-well plates. Upper micrograph shows control DMSO-treated cells while lower micrograph represents BX795-treated cells. Scale bar represents 150 μm. D. Tests of the four hit compounds in a dose-response format. Data are presented as mean ± SEM.

Techniques Used: High Content Screening, Derivative Assay, Expressing

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    R&D Systems bdnf
    Representation of the BNDF location and structure. The Val66Met (rs6265) polymorphism of the <t>BDNF</t> gene consists of a substitution of valine for methionine in the BDNF prodomain. BDNF exons are represented by boxes noted with roman algorisms, while lines represent introns. The SNP locus is in the prodomain region of the IX exon. CDS coding DNA sequence. pA polyadenylation sites. ATG site initiation codon. BDNF brain-derived neurotrophic factor; Val/Val Val66Val homozygous. Val/Met Val66Met heterozygous.
    Bdnf, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bdnf/product/R&D Systems
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
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    R&D Systems quantikine human free bdnf elisa kit
    Representation of the BNDF location and structure. The Val66Met (rs6265) polymorphism of the <t>BDNF</t> gene consists of a substitution of valine for methionine in the BDNF prodomain. BDNF exons are represented by boxes noted with roman algorisms, while lines represent introns. The SNP locus is in the prodomain region of the IX exon. CDS coding DNA sequence. pA polyadenylation sites. ATG site initiation codon. BDNF brain-derived neurotrophic factor; Val/Val Val66Val homozygous. Val/Met Val66Met heterozygous.
    Quantikine Human Free Bdnf Elisa Kit, supplied by R&D Systems, 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/result/quantikine human free bdnf elisa kit/product/R&D Systems
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    quantikine human free bdnf elisa kit - by Bioz Stars, 2022-12
    91/100 stars
      Buy from Supplier

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    Representation of the BNDF location and structure. The Val66Met (rs6265) polymorphism of the BDNF gene consists of a substitution of valine for methionine in the BDNF prodomain. BDNF exons are represented by boxes noted with roman algorisms, while lines represent introns. The SNP locus is in the prodomain region of the IX exon. CDS coding DNA sequence. pA polyadenylation sites. ATG site initiation codon. BDNF brain-derived neurotrophic factor; Val/Val Val66Val homozygous. Val/Met Val66Met heterozygous.

    Journal: Scientific Reports

    Article Title: Functional connectivity response to acute pain assessed by fNIRS is associated with BDNF genotype in fibromyalgia: an exploratory study

    doi: 10.1038/s41598-022-23476-3

    Figure Lengend Snippet: Representation of the BNDF location and structure. The Val66Met (rs6265) polymorphism of the BDNF gene consists of a substitution of valine for methionine in the BDNF prodomain. BDNF exons are represented by boxes noted with roman algorisms, while lines represent introns. The SNP locus is in the prodomain region of the IX exon. CDS coding DNA sequence. pA polyadenylation sites. ATG site initiation codon. BDNF brain-derived neurotrophic factor; Val/Val Val66Val homozygous. Val/Met Val66Met heterozygous.

    Article Snippet: The BDNF serum levels were assessed by enzyme-linked immunosorbent assay (ELISA) monoclonal antibodies specific for BDNF (R & D Systems, MN, United States, ChemiKine BDNF Sandwich ELISA kit, CYT306, Chemicon/Millipore, Billerica, MA, USA), and the Enzyme-linked Immunosorbent.

    Techniques: Sequencing, Derivative Assay

    The difference in functional connectivity patterns in response to acute pain according to the BDNF genotype and its associations. The Val66Met (rs6265) polymorphism of the BDNF gene impacts the changes in FC in response to a cold pressor test in female fibromyalgia patients. Heatmaps presenting the difference in 7 min of resting-state functional connectivity assessed after and before a cold pressor test, in the Val/Val and Val/Met groups. The significant differences between groups of BDNF genotypes are presented with an asterisk. ( A ) Data regarding the Val/Val group. The blue edges between regions of interest represent a significant decrease in ΔFC between groups. ( B ) Data regarding the Val/Met group. The red edges represent a significant increase in ΔFC between groups. ( C ) Data associated with the Val/Met group. The Val/Met group presented a significantly ΔFC difference in response to acute pain in the cold pressor test, coupled with lower disability due to pain and performance associated with higher efficiency of the descending pain modulatory system assessed by the conditioned pain modulation test. The colored edges represent ΔFC values as indicated in the heatmap bar. BDNF brain-derived neurotrophic factor. Val/Val Val66Val homozygous. Val/Met Val66Met heterozygous. ΔFC functional connectivity delta-value. rs-FC resting state functional connectivity. PFC prefrontal cortex. MC motor cortex. -l left. -r right. * p

    Journal: Scientific Reports

    Article Title: Functional connectivity response to acute pain assessed by fNIRS is associated with BDNF genotype in fibromyalgia: an exploratory study

    doi: 10.1038/s41598-022-23476-3

    Figure Lengend Snippet: The difference in functional connectivity patterns in response to acute pain according to the BDNF genotype and its associations. The Val66Met (rs6265) polymorphism of the BDNF gene impacts the changes in FC in response to a cold pressor test in female fibromyalgia patients. Heatmaps presenting the difference in 7 min of resting-state functional connectivity assessed after and before a cold pressor test, in the Val/Val and Val/Met groups. The significant differences between groups of BDNF genotypes are presented with an asterisk. ( A ) Data regarding the Val/Val group. The blue edges between regions of interest represent a significant decrease in ΔFC between groups. ( B ) Data regarding the Val/Met group. The red edges represent a significant increase in ΔFC between groups. ( C ) Data associated with the Val/Met group. The Val/Met group presented a significantly ΔFC difference in response to acute pain in the cold pressor test, coupled with lower disability due to pain and performance associated with higher efficiency of the descending pain modulatory system assessed by the conditioned pain modulation test. The colored edges represent ΔFC values as indicated in the heatmap bar. BDNF brain-derived neurotrophic factor. Val/Val Val66Val homozygous. Val/Met Val66Met heterozygous. ΔFC functional connectivity delta-value. rs-FC resting state functional connectivity. PFC prefrontal cortex. MC motor cortex. -l left. -r right. * p

    Article Snippet: The BDNF serum levels were assessed by enzyme-linked immunosorbent assay (ELISA) monoclonal antibodies specific for BDNF (R & D Systems, MN, United States, ChemiKine BDNF Sandwich ELISA kit, CYT306, Chemicon/Millipore, Billerica, MA, USA), and the Enzyme-linked Immunosorbent.

    Techniques: Functional Assay, Derivative Assay