rabbit monoclonal anti stmn1  (Cell Signaling Technology Inc)

 
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    Name:
    β Actin Antibody
    Description:
    Actin a ubiquitous eukaryotic protein is the major component of the cytoskeleton At least six isoforms are known in mammals Nonmuscle β and γ actin also known as cytoplasmic actin are predominantly expressed in nonmuscle cells controlling cell structure and motility 1 α cardiac and α skeletal actin are expressed in striated cardiac and skeletal muscles respectively two smooth muscle actins α and γ actin are found primarily in vascular smooth muscle and enteric smooth muscle respectively These actin isoforms regulate the contractile potential of muscle cells 1 Actin exists mainly as a fibrous polymer F actin In response to cytoskeletal reorganizing signals during processes such as cytokinesis endocytosis or stress cofilin promotes fragmentation and depolymerization of F actin resulting in an increase in the monomeric globular form G actin 2 The ARP2 3 complex stabilizes F actin fragments and promotes formation of new actin filaments 2 Research studies have shown that actin is hyperphosphorylated in primary breast tumors 3 Cleavage of actin under apoptotic conditions has been observed in vitro and in cardiac and skeletal muscle as shown in research studies 4 6 Actin cleavage by caspase 3 may accelerate ubiquitin proteasome dependent muscle proteolysis 6
    Catalog Number:
    4967
    Price:
    None
    Applications:
    Western Blot
    Category:
    Primary Antibodies
    Source:
    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to amino-terminal residues of human β-actin. Antibodies are purified by protein A and peptide affinity chromatography.
    Reactivity:
    Human Mouse Rat Hamster Monkey Mink D melanogaster Zebrafish Bovine
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    Structured Review

    Cell Signaling Technology Inc rabbit monoclonal anti stmn1
    Model of how SUMOylation of KIF4A enhances binding to MT destabilizer <t>STMN1</t> and promotes abscission. Cartoon depicting the intercellular bridge between the newly formed daughter cells during cytokinesis. (I) In cells expressing wild-type KIF4A, SUMOylation of KIF4A enhances its binding to STMN1 at the midbody. Subsequently, MT destabilization by STMN1 is promoted, which results in abscission and thereby completion of the final step of cell division. (II) Blocking KIF4A SUMOylation reduces STMN1 binding. Consequently, this results in reduced MT destabilization by STMN1 at the midbody and ensuing delay in abscission.
    Actin a ubiquitous eukaryotic protein is the major component of the cytoskeleton At least six isoforms are known in mammals Nonmuscle β and γ actin also known as cytoplasmic actin are predominantly expressed in nonmuscle cells controlling cell structure and motility 1 α cardiac and α skeletal actin are expressed in striated cardiac and skeletal muscles respectively two smooth muscle actins α and γ actin are found primarily in vascular smooth muscle and enteric smooth muscle respectively These actin isoforms regulate the contractile potential of muscle cells 1 Actin exists mainly as a fibrous polymer F actin In response to cytoskeletal reorganizing signals during processes such as cytokinesis endocytosis or stress cofilin promotes fragmentation and depolymerization of F actin resulting in an increase in the monomeric globular form G actin 2 The ARP2 3 complex stabilizes F actin fragments and promotes formation of new actin filaments 2 Research studies have shown that actin is hyperphosphorylated in primary breast tumors 3 Cleavage of actin under apoptotic conditions has been observed in vitro and in cardiac and skeletal muscle as shown in research studies 4 6 Actin cleavage by caspase 3 may accelerate ubiquitin proteasome dependent muscle proteolysis 6
    https://www.bioz.com/result/rabbit monoclonal anti stmn1/product/Cell Signaling Technology Inc
    Average 84 stars, based on 2761 article reviews
    Price from $9.99 to $1999.99
    rabbit monoclonal anti stmn1 - by Bioz Stars, 2020-09
    84/100 stars

    Images

    1) Product Images from "Chromokinesin KIF4A teams up with stathmin 1 to regulate abscission in a SUMO-dependent manner"

    Article Title: Chromokinesin KIF4A teams up with stathmin 1 to regulate abscission in a SUMO-dependent manner

    Journal: Journal of Cell Science

    doi: 10.1242/jcs.248591

    Model of how SUMOylation of KIF4A enhances binding to MT destabilizer STMN1 and promotes abscission. Cartoon depicting the intercellular bridge between the newly formed daughter cells during cytokinesis. (I) In cells expressing wild-type KIF4A, SUMOylation of KIF4A enhances its binding to STMN1 at the midbody. Subsequently, MT destabilization by STMN1 is promoted, which results in abscission and thereby completion of the final step of cell division. (II) Blocking KIF4A SUMOylation reduces STMN1 binding. Consequently, this results in reduced MT destabilization by STMN1 at the midbody and ensuing delay in abscission.
    Figure Legend Snippet: Model of how SUMOylation of KIF4A enhances binding to MT destabilizer STMN1 and promotes abscission. Cartoon depicting the intercellular bridge between the newly formed daughter cells during cytokinesis. (I) In cells expressing wild-type KIF4A, SUMOylation of KIF4A enhances its binding to STMN1 at the midbody. Subsequently, MT destabilization by STMN1 is promoted, which results in abscission and thereby completion of the final step of cell division. (II) Blocking KIF4A SUMOylation reduces STMN1 binding. Consequently, this results in reduced MT destabilization by STMN1 at the midbody and ensuing delay in abscission.

    Techniques Used: Binding Assay, Expressing, Blocking Assay

    SUMOylation of KIF4A enhances binding to STMN1. (A) A cartoon depicting the experimental set-up to identify proteins binding preferentially to SUMOylated KIF4A. Recombinant GST–KIF4A WT or its SUMOylation-deficient mutant (K460R) were bound to beads and in vitro SUMOylation assays were performed. In control assays, SUMO2 was omitted. Subsequently, U2OS cell lysates were added, incubation was performed, samples were washed and bound proteins were identified by mass spectrometry. (B) Volcano plot showing proteins binding preferentially to SUMOylated over non-SUMOylated GST–KIF4A. On the x -axis, the Log2 fold change (FC) between the proteins identified by mass spectrometry in the samples bound to SUMOylated GST–KIF4A WT versus non-SUMOylated GST–KIF4A WT is indicated. On the y -axis, the −Log10( P ) values for the identified proteins are shown. All proteins above the dashed line were considered significantly different between the two datasets ( P
    Figure Legend Snippet: SUMOylation of KIF4A enhances binding to STMN1. (A) A cartoon depicting the experimental set-up to identify proteins binding preferentially to SUMOylated KIF4A. Recombinant GST–KIF4A WT or its SUMOylation-deficient mutant (K460R) were bound to beads and in vitro SUMOylation assays were performed. In control assays, SUMO2 was omitted. Subsequently, U2OS cell lysates were added, incubation was performed, samples were washed and bound proteins were identified by mass spectrometry. (B) Volcano plot showing proteins binding preferentially to SUMOylated over non-SUMOylated GST–KIF4A. On the x -axis, the Log2 fold change (FC) between the proteins identified by mass spectrometry in the samples bound to SUMOylated GST–KIF4A WT versus non-SUMOylated GST–KIF4A WT is indicated. On the y -axis, the −Log10( P ) values for the identified proteins are shown. All proteins above the dashed line were considered significantly different between the two datasets ( P

    Techniques Used: Binding Assay, Recombinant, Mutagenesis, In Vitro, Incubation, Mass Spectrometry

    2) Product Images from "Hispidin induces autophagic and necrotic death in SGC-7901 gastric cancer cells through lysosomal membrane permeabilization by inhibiting tubulin polymerization"

    Article Title: Hispidin induces autophagic and necrotic death in SGC-7901 gastric cancer cells through lysosomal membrane permeabilization by inhibiting tubulin polymerization

    Journal: Oncotarget

    doi: 10.18632/oncotarget.15935

    STMN1 phosphorylation and dephosphorylation is involved in hispidin-induced microtubule depolymerization ( A and B ) Tubulin was purified, cross-linked and used as a receptor in hispidin and paclitaxel binding assays. ( C ) SGC-7901 and GES-1 cells were incubated with hispidin or 0.1% DMSO. Then, STMN1 phosphorylation at ser 16 was detected by Western blotting using β-actin as an internal control. ( D ) SGC-7901 cells were transfected with scrambled RNA and STMN1 RNA for 48 h, and STMN1 levels were determined by Western blot. ( E ) The transfected cells were treated with 122 μM hispidin and assayed for viability.
    Figure Legend Snippet: STMN1 phosphorylation and dephosphorylation is involved in hispidin-induced microtubule depolymerization ( A and B ) Tubulin was purified, cross-linked and used as a receptor in hispidin and paclitaxel binding assays. ( C ) SGC-7901 and GES-1 cells were incubated with hispidin or 0.1% DMSO. Then, STMN1 phosphorylation at ser 16 was detected by Western blotting using β-actin as an internal control. ( D ) SGC-7901 cells were transfected with scrambled RNA and STMN1 RNA for 48 h, and STMN1 levels were determined by Western blot. ( E ) The transfected cells were treated with 122 μM hispidin and assayed for viability.

    Techniques Used: De-Phosphorylation Assay, Purification, Binding Assay, Incubation, Western Blot, Transfection

    Hispidin induces necrotic cell death involving autophagy in SGC-7901 cells ( A ) SGC-7901 cells were treated with hispidin or rapamycin. Then, LC3-I and LC3-II were detected by Western blotting using β-actin as an internal control. ( B ) SGC-7901 cells were transiently transfected with mCherry-GFP-LC3B and treated with hispidin, 3-MA, or rapamycin containing medium. The colocalization of GFP and mCherry signals was analyzed. Quantitation represents the number of autophagosomes and autolysosomes per cell ( n = 20). ( C ) After preincubation with either 10 mM 3-Methyladenine (3-MA), 100 nM wortmannin, 100 μM hydroxychloroquine, 100 nM bafilomycin A1, 10 μg/mL pepstatin A or 10 μg/mL E64d SGC-7901 cells were treated with 122 μM hispidin and assayed for cell viability. ( D and E ) SGC-7901 cells were transfected with scrambled RNA and ATG5 RNA for 48 h, and ATG levels were determined by Western blot; cell viability was assayed using MTT. ( F ) SGC-7901 cells were preincubated in the presence or absence of 25, 50 or 100 nM necrostatin-1 for 2 h before being treated with 122 μM hispidin. Then, the cells were examined for viability. ( G ) Transmission electron microscopy of SGC-7901 cells. Cells were treated with 122 μM hispidin.
    Figure Legend Snippet: Hispidin induces necrotic cell death involving autophagy in SGC-7901 cells ( A ) SGC-7901 cells were treated with hispidin or rapamycin. Then, LC3-I and LC3-II were detected by Western blotting using β-actin as an internal control. ( B ) SGC-7901 cells were transiently transfected with mCherry-GFP-LC3B and treated with hispidin, 3-MA, or rapamycin containing medium. The colocalization of GFP and mCherry signals was analyzed. Quantitation represents the number of autophagosomes and autolysosomes per cell ( n = 20). ( C ) After preincubation with either 10 mM 3-Methyladenine (3-MA), 100 nM wortmannin, 100 μM hydroxychloroquine, 100 nM bafilomycin A1, 10 μg/mL pepstatin A or 10 μg/mL E64d SGC-7901 cells were treated with 122 μM hispidin and assayed for cell viability. ( D and E ) SGC-7901 cells were transfected with scrambled RNA and ATG5 RNA for 48 h, and ATG levels were determined by Western blot; cell viability was assayed using MTT. ( F ) SGC-7901 cells were preincubated in the presence or absence of 25, 50 or 100 nM necrostatin-1 for 2 h before being treated with 122 μM hispidin. Then, the cells were examined for viability. ( G ) Transmission electron microscopy of SGC-7901 cells. Cells were treated with 122 μM hispidin.

    Techniques Used: Western Blot, Transfection, Quantitation Assay, MTT Assay, Transmission Assay, Electron Microscopy

    Hispidin induces caspase-independent cell death in SGC-7901 cells ( A ) Chemical structure of hispidin. Cells were incubated with hispidin (41, 82 or 122 μM) or 0.1% DMSO for 12, 24, 48 or 72 h. The viability of SGC-7901 ( B ) and GES-1 ( C ) cells was determined using the MTT assay. ( D ) Cells were incubated with hispidin or 0.1% DMSO and then were assayed for phosphatidyl serine externalization and PI permeability. ( E ) SGC-7901 cells were treated with 41, 81, or 122 μM hispidin; 0.1% DMSO; or 3.4 μM Adriamycin for 6 h. Then, caspase activity was examined. ( F ) SGC-7901 cells were treated with hispidin or Adriamycin. Then, caspase-3, caspase-8 and caspase-9 were detected by Western blotting using β-actin as an internal control. ( G ) SGC-7901 cells were preincubated in the presence or absence of 25 or 50 μM z-VAD-FMK for 2 h before being treated with 122 μM hispidin. Then, the cells were examined for PI permeability.
    Figure Legend Snippet: Hispidin induces caspase-independent cell death in SGC-7901 cells ( A ) Chemical structure of hispidin. Cells were incubated with hispidin (41, 82 or 122 μM) or 0.1% DMSO for 12, 24, 48 or 72 h. The viability of SGC-7901 ( B ) and GES-1 ( C ) cells was determined using the MTT assay. ( D ) Cells were incubated with hispidin or 0.1% DMSO and then were assayed for phosphatidyl serine externalization and PI permeability. ( E ) SGC-7901 cells were treated with 41, 81, or 122 μM hispidin; 0.1% DMSO; or 3.4 μM Adriamycin for 6 h. Then, caspase activity was examined. ( F ) SGC-7901 cells were treated with hispidin or Adriamycin. Then, caspase-3, caspase-8 and caspase-9 were detected by Western blotting using β-actin as an internal control. ( G ) SGC-7901 cells were preincubated in the presence or absence of 25 or 50 μM z-VAD-FMK for 2 h before being treated with 122 μM hispidin. Then, the cells were examined for PI permeability.

    Techniques Used: Incubation, MTT Assay, Permeability, Activity Assay, Western Blot

    3) Product Images from "Loss of Cytoplasmic CDK1 Predicts Poor Survival in Human Lung Cancer and Confers Chemotherapeutic Resistance"

    Article Title: Loss of Cytoplasmic CDK1 Predicts Poor Survival in Human Lung Cancer and Confers Chemotherapeutic Resistance

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0023849

    Loss of CDK1 protein and activity and chemotherapeutic resistance. A. FT210 cells were serum-starvated in 0.1% FBS RPMI1640 medium overnight, then treated with 10 µM etoposide or cisplatin in 0.1% FBS containing medium for 4 days at 32°C or 39°C. Apoptosis (sub-G1 DNA content) was determined by flow cytometry (C: Control; T: Treatment). B. FT210 cells were cultured in normal medium and treated with 1 µM paclitaxel or docetaxel and 0.1 µM vinorelbine for 1–4 Days. The CDK1 protein was detected at Day 3 using CDK1 or p-Y15 CDK1 antibodies, and apoptotic death was monitored by PARP cleavage. Apoptosis was determined at Day 4. C. FT210 and its parental cell line FM3A cells were cultured for 6 h then subjected to subcellular fractionation for immunoblotting analysis. αTubulin and p53 served as loading controls for cytoplasmic and nuclear fractions, respectively. D. FM3A and FT210 cells were cultured at 39°C for 72 h and subjected to subcellular fractionation. Expression of CDK1, p-Survivin (Thr34) and Survivin was assessed by immunoblotting. E. FM3A and FT210 cells were treated with 1 µM paclitaxel or docetaxel and 0.1 µM vinorelbine. Apoptosis was determined at Day 4.
    Figure Legend Snippet: Loss of CDK1 protein and activity and chemotherapeutic resistance. A. FT210 cells were serum-starvated in 0.1% FBS RPMI1640 medium overnight, then treated with 10 µM etoposide or cisplatin in 0.1% FBS containing medium for 4 days at 32°C or 39°C. Apoptosis (sub-G1 DNA content) was determined by flow cytometry (C: Control; T: Treatment). B. FT210 cells were cultured in normal medium and treated with 1 µM paclitaxel or docetaxel and 0.1 µM vinorelbine for 1–4 Days. The CDK1 protein was detected at Day 3 using CDK1 or p-Y15 CDK1 antibodies, and apoptotic death was monitored by PARP cleavage. Apoptosis was determined at Day 4. C. FT210 and its parental cell line FM3A cells were cultured for 6 h then subjected to subcellular fractionation for immunoblotting analysis. αTubulin and p53 served as loading controls for cytoplasmic and nuclear fractions, respectively. D. FM3A and FT210 cells were cultured at 39°C for 72 h and subjected to subcellular fractionation. Expression of CDK1, p-Survivin (Thr34) and Survivin was assessed by immunoblotting. E. FM3A and FT210 cells were treated with 1 µM paclitaxel or docetaxel and 0.1 µM vinorelbine. Apoptosis was determined at Day 4.

    Techniques Used: Activity Assay, Flow Cytometry, Cytometry, Cell Culture, Fractionation, Expressing

    Modulation of CDK1 protein level and activity and sensitivity of NSCLC cells to Paclitaxel treatment. A. CDK1 protein over or under expressed in H157 cells. Cells were transfected with CDK1 plasmid or siRNA, 48 h or 72 h later, were treated with 1 µM paclitaxel for 2 days. CDK1 protein level was monitored by CDK1 or p-Y15 CDK1 antibodies. Sub-G1 DNA content was determined by flow cytometry. B. Knockdown of CDK1 in A549 cells. Cells were transfected with CDK1 siRNA, 72 h later, treated with 1 µM paclitaxel for 2 days. Apoptosis was determined by PARP cleavage using immunoblotting or sub-G1 DNA content using flow cytometry. CDK1 protein level was monitored by CDK1 or p-Y15 CDK1 antibodies. C. Overexpression of CDK1 or CDK1DN in A549 cells. Cells were transfected with CDK1 or CDK1DN plasmids, 48 h later, cell cycling stopped by overnight pretreatment of low serum (0.1% FBS) medium with PI3K inhibitor LY294002 (10 µM), then cells were treated with 1 µM paclitaxel in low serum medium containing LY294002 (10 µM, freshly added) for 2 days. Sub-G1 fraction and cell cycle profile were determined by flow cytometry. Over expression of CDK1 and CDK1DN was detected by CDK1 antibody.
    Figure Legend Snippet: Modulation of CDK1 protein level and activity and sensitivity of NSCLC cells to Paclitaxel treatment. A. CDK1 protein over or under expressed in H157 cells. Cells were transfected with CDK1 plasmid or siRNA, 48 h or 72 h later, were treated with 1 µM paclitaxel for 2 days. CDK1 protein level was monitored by CDK1 or p-Y15 CDK1 antibodies. Sub-G1 DNA content was determined by flow cytometry. B. Knockdown of CDK1 in A549 cells. Cells were transfected with CDK1 siRNA, 72 h later, treated with 1 µM paclitaxel for 2 days. Apoptosis was determined by PARP cleavage using immunoblotting or sub-G1 DNA content using flow cytometry. CDK1 protein level was monitored by CDK1 or p-Y15 CDK1 antibodies. C. Overexpression of CDK1 or CDK1DN in A549 cells. Cells were transfected with CDK1 or CDK1DN plasmids, 48 h later, cell cycling stopped by overnight pretreatment of low serum (0.1% FBS) medium with PI3K inhibitor LY294002 (10 µM), then cells were treated with 1 µM paclitaxel in low serum medium containing LY294002 (10 µM, freshly added) for 2 days. Sub-G1 fraction and cell cycle profile were determined by flow cytometry. Over expression of CDK1 and CDK1DN was detected by CDK1 antibody.

    Techniques Used: Activity Assay, Transfection, Plasmid Preparation, Flow Cytometry, Cytometry, Over Expression

    Dual role of CDK1 in tumorigenesis and chemotherapeutic sensitivity. A. A model of CDK1 activation. When inactive p-Y15/T14 CDK1 is dephosphorylated on Y15 and T14 by CDC25A, it associates with Cyclin A/B and becomes active within the cytoplasm, then quickly translocates into the nucleus, where it promotes G1 to S and G2/M transitions. Active CDK1 is inactivated via sequential phosphorylation of Y15 and T14 by Wee1 and Myt1, and sequestrated by 14-3-3σ in the cytoplasm. This process repeats with cell cycling to drive cellular proliferation. B. A diagram to illustrate the dual role of CDK1 as a tumorigenic driver in lung carcinogenesis and a sensitizer in chemotherapeutic responsiveness.
    Figure Legend Snippet: Dual role of CDK1 in tumorigenesis and chemotherapeutic sensitivity. A. A model of CDK1 activation. When inactive p-Y15/T14 CDK1 is dephosphorylated on Y15 and T14 by CDC25A, it associates with Cyclin A/B and becomes active within the cytoplasm, then quickly translocates into the nucleus, where it promotes G1 to S and G2/M transitions. Active CDK1 is inactivated via sequential phosphorylation of Y15 and T14 by Wee1 and Myt1, and sequestrated by 14-3-3σ in the cytoplasm. This process repeats with cell cycling to drive cellular proliferation. B. A diagram to illustrate the dual role of CDK1 as a tumorigenic driver in lung carcinogenesis and a sensitizer in chemotherapeutic responsiveness.

    Techniques Used: Activation Assay

    Tissue microarray immunohistochemistry. A. Examples of CDK1, PTTG1, Survivin and TOP2A subcellular staining in clinical tumor samples (-C: cytoplasmic staining; -N: nuclear staining). Staining is shown at 400× magnification. B. Tissue distribution of positive rates for CDK1, PTTG1, Survivin and TOP2A. AD: Adenocarcinoma; SCC: Squamous cell carcinoma; N-AD: Adjacent non-diseased lung tissues from Adenocarcinoma; N-SCC: Adjacent non-diseased lung tissues from squamous cell carcinoma; N-O: Non-pulmonary normal organs. C. Overview of entire tissue microarray staining for expression of these antigens in the cytoplasm or nucleus.
    Figure Legend Snippet: Tissue microarray immunohistochemistry. A. Examples of CDK1, PTTG1, Survivin and TOP2A subcellular staining in clinical tumor samples (-C: cytoplasmic staining; -N: nuclear staining). Staining is shown at 400× magnification. B. Tissue distribution of positive rates for CDK1, PTTG1, Survivin and TOP2A. AD: Adenocarcinoma; SCC: Squamous cell carcinoma; N-AD: Adjacent non-diseased lung tissues from Adenocarcinoma; N-SCC: Adjacent non-diseased lung tissues from squamous cell carcinoma; N-O: Non-pulmonary normal organs. C. Overview of entire tissue microarray staining for expression of these antigens in the cytoplasm or nucleus.

    Techniques Used: Microarray, Immunohistochemistry, Staining, Expressing

    The associations of staining outcomes with tumor samples, clinical factors and patient survival. A. The hierarchial clustering for both antibodies and tumors using Cluster 3.0 and Java TreeView. B. The positive rates of CDK1, PTTG1, Survivin and TOP2A in early stages (1–2) and advanced stages (3–4). C. Kaplan-Meier survival analysis for cytoplasmic CDK1 staining pattern in NSCLC. The permutation test was used to calculate the p value for all tumors and tumors by stage.
    Figure Legend Snippet: The associations of staining outcomes with tumor samples, clinical factors and patient survival. A. The hierarchial clustering for both antibodies and tumors using Cluster 3.0 and Java TreeView. B. The positive rates of CDK1, PTTG1, Survivin and TOP2A in early stages (1–2) and advanced stages (3–4). C. Kaplan-Meier survival analysis for cytoplasmic CDK1 staining pattern in NSCLC. The permutation test was used to calculate the p value for all tumors and tumors by stage.

    Techniques Used: Staining

    4) Product Images from "A Cohort Study of STMN1 Expression in Colorectal Cancer: Body Mass Index and Prognosis"

    Article Title: A Cohort Study of STMN1 Expression in Colorectal Cancer: Body Mass Index and Prognosis

    Journal: The American journal of gastroenterology

    doi: 10.1038/ajg.2009.281

    Modifying effect of BMI on the relation between STMN1 and mortality
    Figure Legend Snippet: Modifying effect of BMI on the relation between STMN1 and mortality

    Techniques Used:

    Effect of obesity on survival in strata of STMN1
    Figure Legend Snippet: Effect of obesity on survival in strata of STMN1

    Techniques Used:

    STMN1 expression in colorectal cancer and patient survival
    Figure Legend Snippet: STMN1 expression in colorectal cancer and patient survival

    Techniques Used: Expressing

    STMN1 status and colorectal cancer mortality in various strata. Log e (adjusted HRs) with 95% CI for colorectal cancer–specific mortality in STMN1 + tumors (vs. STMN–tumors) are shown. CI, confidence interval; CIMP, CpG island methylator
    Figure Legend Snippet: STMN1 status and colorectal cancer mortality in various strata. Log e (adjusted HRs) with 95% CI for colorectal cancer–specific mortality in STMN1 + tumors (vs. STMN–tumors) are shown. CI, confidence interval; CIMP, CpG island methylator

    Techniques Used:

    STMN1 expression in colorectal cancer and patient survival
    Figure Legend Snippet: STMN1 expression in colorectal cancer and patient survival

    Techniques Used: Expressing

    STMN1 expression in colorectal cancer cells. ( a ) Negative for STMN1 expression in colorectal cancer (arrows). Weak staining in inflammatory cells serves as an internal positive control (empty arrows). ( b ) Positive for STMN1 expression in colorectal cancer
    Figure Legend Snippet: STMN1 expression in colorectal cancer cells. ( a ) Negative for STMN1 expression in colorectal cancer (arrows). Weak staining in inflammatory cells serves as an internal positive control (empty arrows). ( b ) Positive for STMN1 expression in colorectal cancer

    Techniques Used: Expressing, Staining, Positive Control

    5) Product Images from "Stathmin and phospho-stathmin protein signature is associated with survival outcomes of breast cancer patients"

    Article Title: Stathmin and phospho-stathmin protein signature is associated with survival outcomes of breast cancer patients

    Journal: Oncotarget

    doi:

    Identification by immunohistochemistry (IHC) of STMN1 and its multiple phosphor-sites in the primary tumor and Kaplan-Meier analysis of DFS in breast cancer patients with high or low STMN1 expression and the expression of its multiple serine phospho-sites A. Representative IHC staining of high and low expression of STMN1 in the large (400×) and small images (100×). B. Representative IHC staining of high and low expression of multiple phosphor-sites (Ser-16, Ser-25, Ser38, Ser63) in the large (400×) and small images (100×). C. Kaplan-Meier analysis of DFS in the training set. D. Kaplan-Meier analysis of DFS in the validation set.
    Figure Legend Snippet: Identification by immunohistochemistry (IHC) of STMN1 and its multiple phosphor-sites in the primary tumor and Kaplan-Meier analysis of DFS in breast cancer patients with high or low STMN1 expression and the expression of its multiple serine phospho-sites A. Representative IHC staining of high and low expression of STMN1 in the large (400×) and small images (100×). B. Representative IHC staining of high and low expression of multiple phosphor-sites (Ser-16, Ser-25, Ser38, Ser63) in the large (400×) and small images (100×). C. Kaplan-Meier analysis of DFS in the training set. D. Kaplan-Meier analysis of DFS in the validation set.

    Techniques Used: Immunohistochemistry, Expressing, Staining

    6) Product Images from "Loss of Cytoplasmic CDK1 Predicts Poor Survival in Human Lung Cancer and Confers Chemotherapeutic Resistance"

    Article Title: Loss of Cytoplasmic CDK1 Predicts Poor Survival in Human Lung Cancer and Confers Chemotherapeutic Resistance

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0023849

    Loss of CDK1 protein and activity and chemotherapeutic resistance. A. FT210 cells were serum-starvated in 0.1% FBS RPMI1640 medium overnight, then treated with 10 µM etoposide or cisplatin in 0.1% FBS containing medium for 4 days at 32°C or 39°C. Apoptosis (sub-G1 DNA content) was determined by flow cytometry (C: Control; T: Treatment). B. FT210 cells were cultured in normal medium and treated with 1 µM paclitaxel or docetaxel and 0.1 µM vinorelbine for 1–4 Days. The CDK1 protein was detected at Day 3 using CDK1 or p-Y15 CDK1 antibodies, and apoptotic death was monitored by PARP cleavage. Apoptosis was determined at Day 4. C. FT210 and its parental cell line FM3A cells were cultured for 6 h then subjected to subcellular fractionation for immunoblotting analysis. αTubulin and p53 served as loading controls for cytoplasmic and nuclear fractions, respectively. D. FM3A and FT210 cells were cultured at 39°C for 72 h and subjected to subcellular fractionation. Expression of CDK1, p-Survivin (Thr34) and Survivin was assessed by immunoblotting. E. FM3A and FT210 cells were treated with 1 µM paclitaxel or docetaxel and 0.1 µM vinorelbine. Apoptosis was determined at Day 4.
    Figure Legend Snippet: Loss of CDK1 protein and activity and chemotherapeutic resistance. A. FT210 cells were serum-starvated in 0.1% FBS RPMI1640 medium overnight, then treated with 10 µM etoposide or cisplatin in 0.1% FBS containing medium for 4 days at 32°C or 39°C. Apoptosis (sub-G1 DNA content) was determined by flow cytometry (C: Control; T: Treatment). B. FT210 cells were cultured in normal medium and treated with 1 µM paclitaxel or docetaxel and 0.1 µM vinorelbine for 1–4 Days. The CDK1 protein was detected at Day 3 using CDK1 or p-Y15 CDK1 antibodies, and apoptotic death was monitored by PARP cleavage. Apoptosis was determined at Day 4. C. FT210 and its parental cell line FM3A cells were cultured for 6 h then subjected to subcellular fractionation for immunoblotting analysis. αTubulin and p53 served as loading controls for cytoplasmic and nuclear fractions, respectively. D. FM3A and FT210 cells were cultured at 39°C for 72 h and subjected to subcellular fractionation. Expression of CDK1, p-Survivin (Thr34) and Survivin was assessed by immunoblotting. E. FM3A and FT210 cells were treated with 1 µM paclitaxel or docetaxel and 0.1 µM vinorelbine. Apoptosis was determined at Day 4.

    Techniques Used: Activity Assay, Flow Cytometry, Cytometry, Cell Culture, Fractionation, Expressing

    Tissue microarray immunohistochemistry. A. Examples of CDK1, PTTG1, Survivin and TOP2A subcellular staining in clinical tumor samples (-C: cytoplasmic staining; -N: nuclear staining). Staining is shown at 400× magnification. B. Tissue distribution of positive rates for CDK1, PTTG1, Survivin and TOP2A. AD: Adenocarcinoma; SCC: Squamous cell carcinoma; N-AD: Adjacent non-diseased lung tissues from Adenocarcinoma; N-SCC: Adjacent non-diseased lung tissues from squamous cell carcinoma; N-O: Non-pulmonary normal organs. C. Overview of entire tissue microarray staining for expression of these antigens in the cytoplasm or nucleus.
    Figure Legend Snippet: Tissue microarray immunohistochemistry. A. Examples of CDK1, PTTG1, Survivin and TOP2A subcellular staining in clinical tumor samples (-C: cytoplasmic staining; -N: nuclear staining). Staining is shown at 400× magnification. B. Tissue distribution of positive rates for CDK1, PTTG1, Survivin and TOP2A. AD: Adenocarcinoma; SCC: Squamous cell carcinoma; N-AD: Adjacent non-diseased lung tissues from Adenocarcinoma; N-SCC: Adjacent non-diseased lung tissues from squamous cell carcinoma; N-O: Non-pulmonary normal organs. C. Overview of entire tissue microarray staining for expression of these antigens in the cytoplasm or nucleus.

    Techniques Used: Microarray, Immunohistochemistry, Staining, Expressing

    The associations of staining outcomes with tumor samples, clinical factors and patient survival. A. The hierarchial clustering for both antibodies and tumors using Cluster 3.0 and Java TreeView. B. The positive rates of CDK1, PTTG1, Survivin and TOP2A in early stages (1–2) and advanced stages (3–4). C. Kaplan-Meier survival analysis for cytoplasmic CDK1 staining pattern in NSCLC. The permutation test was used to calculate the p value for all tumors and tumors by stage.
    Figure Legend Snippet: The associations of staining outcomes with tumor samples, clinical factors and patient survival. A. The hierarchial clustering for both antibodies and tumors using Cluster 3.0 and Java TreeView. B. The positive rates of CDK1, PTTG1, Survivin and TOP2A in early stages (1–2) and advanced stages (3–4). C. Kaplan-Meier survival analysis for cytoplasmic CDK1 staining pattern in NSCLC. The permutation test was used to calculate the p value for all tumors and tumors by stage.

    Techniques Used: Staining

    7) Product Images from "Hispidin induces autophagic and necrotic death in SGC-7901 gastric cancer cells through lysosomal membrane permeabilization by inhibiting tubulin polymerization"

    Article Title: Hispidin induces autophagic and necrotic death in SGC-7901 gastric cancer cells through lysosomal membrane permeabilization by inhibiting tubulin polymerization

    Journal: Oncotarget

    doi: 10.18632/oncotarget.15935

    Hispidin induces caspase-independent cell death in SGC-7901 cells ( A ) Chemical structure of hispidin. Cells were incubated with hispidin (41, 82 or 122 μM) or 0.1% DMSO for 12, 24, 48 or 72 h. The viability of SGC-7901 ( B ) and GES-1 ( C ) cells was determined using the MTT assay. ( D ) Cells were incubated with hispidin or 0.1% DMSO and then were assayed for phosphatidyl serine externalization and PI permeability. ( E ) SGC-7901 cells were treated with 41, 81, or 122 μM hispidin; 0.1% DMSO; or 3.4 μM Adriamycin for 6 h. Then, caspase activity was examined. ( F ) SGC-7901 cells were treated with hispidin or Adriamycin. Then, caspase-3, caspase-8 and caspase-9 were detected by Western blotting using β-actin as an internal control. ( G ) SGC-7901 cells were preincubated in the presence or absence of 25 or 50 μM z-VAD-FMK for 2 h before being treated with 122 μM hispidin. Then, the cells were examined for PI permeability.
    Figure Legend Snippet: Hispidin induces caspase-independent cell death in SGC-7901 cells ( A ) Chemical structure of hispidin. Cells were incubated with hispidin (41, 82 or 122 μM) or 0.1% DMSO for 12, 24, 48 or 72 h. The viability of SGC-7901 ( B ) and GES-1 ( C ) cells was determined using the MTT assay. ( D ) Cells were incubated with hispidin or 0.1% DMSO and then were assayed for phosphatidyl serine externalization and PI permeability. ( E ) SGC-7901 cells were treated with 41, 81, or 122 μM hispidin; 0.1% DMSO; or 3.4 μM Adriamycin for 6 h. Then, caspase activity was examined. ( F ) SGC-7901 cells were treated with hispidin or Adriamycin. Then, caspase-3, caspase-8 and caspase-9 were detected by Western blotting using β-actin as an internal control. ( G ) SGC-7901 cells were preincubated in the presence or absence of 25 or 50 μM z-VAD-FMK for 2 h before being treated with 122 μM hispidin. Then, the cells were examined for PI permeability.

    Techniques Used: Incubation, MTT Assay, Permeability, Activity Assay, Western Blot

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    Cell Signaling Technology Inc primary antibody against stmn1
    Modifying effect of BMI on the relation between <t>STMN1</t> and mortality
    Primary Antibody Against Stmn1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Identification by immunohistochemistry (IHC) of <t>STMN1</t> and its multiple phosphor-sites in the primary tumor and Kaplan-Meier analysis of DFS in breast cancer patients with high or low STMN1 expression and the expression of its multiple serine phospho-sites A. Representative IHC staining of high and low expression of STMN1 in the large (400×) and small images (100×). B. Representative IHC staining of high and low expression of multiple phosphor-sites (Ser-16, Ser-25, <t>Ser38,</t> Ser63) in the large (400×) and small images (100×). C. Kaplan-Meier analysis of DFS in the training set. D. Kaplan-Meier analysis of DFS in the validation set.
    Polyclonal Rabbit Anti Human Stmn1 Ser38, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc rabbit anti human stmn1 polyclonal antibodies
    Identification by immunohistochemistry (IHC) of <t>STMN1</t> and its multiple phosphor-sites in the primary tumor and Kaplan-Meier analysis of DFS in breast cancer patients with high or low STMN1 expression and the expression of its multiple serine phospho-sites A. Representative IHC staining of high and low expression of STMN1 in the large (400×) and small images (100×). B. Representative IHC staining of high and low expression of multiple phosphor-sites (Ser-16, Ser-25, <t>Ser38,</t> Ser63) in the large (400×) and small images (100×). C. Kaplan-Meier analysis of DFS in the training set. D. Kaplan-Meier analysis of DFS in the validation set.
    Rabbit Anti Human Stmn1 Polyclonal Antibodies, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Modifying effect of BMI on the relation between STMN1 and mortality

    Journal: The American journal of gastroenterology

    Article Title: A Cohort Study of STMN1 Expression in Colorectal Cancer: Body Mass Index and Prognosis

    doi: 10.1038/ajg.2009.281

    Figure Lengend Snippet: Modifying effect of BMI on the relation between STMN1 and mortality

    Article Snippet: Primary antibody against STMN1 (Rabbit polyclonal to STMN1, 1:50 dilution; Cell Signaling, Danvers, MA) was applied, and the slides were maintained overnight at room temperature.

    Techniques:

    Effect of obesity on survival in strata of STMN1

    Journal: The American journal of gastroenterology

    Article Title: A Cohort Study of STMN1 Expression in Colorectal Cancer: Body Mass Index and Prognosis

    doi: 10.1038/ajg.2009.281

    Figure Lengend Snippet: Effect of obesity on survival in strata of STMN1

    Article Snippet: Primary antibody against STMN1 (Rabbit polyclonal to STMN1, 1:50 dilution; Cell Signaling, Danvers, MA) was applied, and the slides were maintained overnight at room temperature.

    Techniques:

    STMN1 expression in colorectal cancer and patient survival

    Journal: The American journal of gastroenterology

    Article Title: A Cohort Study of STMN1 Expression in Colorectal Cancer: Body Mass Index and Prognosis

    doi: 10.1038/ajg.2009.281

    Figure Lengend Snippet: STMN1 expression in colorectal cancer and patient survival

    Article Snippet: Primary antibody against STMN1 (Rabbit polyclonal to STMN1, 1:50 dilution; Cell Signaling, Danvers, MA) was applied, and the slides were maintained overnight at room temperature.

    Techniques: Expressing

    STMN1 status and colorectal cancer mortality in various strata. Log e (adjusted HRs) with 95% CI for colorectal cancer–specific mortality in STMN1 + tumors (vs. STMN–tumors) are shown. CI, confidence interval; CIMP, CpG island methylator

    Journal: The American journal of gastroenterology

    Article Title: A Cohort Study of STMN1 Expression in Colorectal Cancer: Body Mass Index and Prognosis

    doi: 10.1038/ajg.2009.281

    Figure Lengend Snippet: STMN1 status and colorectal cancer mortality in various strata. Log e (adjusted HRs) with 95% CI for colorectal cancer–specific mortality in STMN1 + tumors (vs. STMN–tumors) are shown. CI, confidence interval; CIMP, CpG island methylator

    Article Snippet: Primary antibody against STMN1 (Rabbit polyclonal to STMN1, 1:50 dilution; Cell Signaling, Danvers, MA) was applied, and the slides were maintained overnight at room temperature.

    Techniques:

    STMN1 expression in colorectal cancer and patient survival

    Journal: The American journal of gastroenterology

    Article Title: A Cohort Study of STMN1 Expression in Colorectal Cancer: Body Mass Index and Prognosis

    doi: 10.1038/ajg.2009.281

    Figure Lengend Snippet: STMN1 expression in colorectal cancer and patient survival

    Article Snippet: Primary antibody against STMN1 (Rabbit polyclonal to STMN1, 1:50 dilution; Cell Signaling, Danvers, MA) was applied, and the slides were maintained overnight at room temperature.

    Techniques: Expressing

    STMN1 expression in colorectal cancer cells. ( a ) Negative for STMN1 expression in colorectal cancer (arrows). Weak staining in inflammatory cells serves as an internal positive control (empty arrows). ( b ) Positive for STMN1 expression in colorectal cancer

    Journal: The American journal of gastroenterology

    Article Title: A Cohort Study of STMN1 Expression in Colorectal Cancer: Body Mass Index and Prognosis

    doi: 10.1038/ajg.2009.281

    Figure Lengend Snippet: STMN1 expression in colorectal cancer cells. ( a ) Negative for STMN1 expression in colorectal cancer (arrows). Weak staining in inflammatory cells serves as an internal positive control (empty arrows). ( b ) Positive for STMN1 expression in colorectal cancer

    Article Snippet: Primary antibody against STMN1 (Rabbit polyclonal to STMN1, 1:50 dilution; Cell Signaling, Danvers, MA) was applied, and the slides were maintained overnight at room temperature.

    Techniques: Expressing, Staining, Positive Control

    Identification by immunohistochemistry (IHC) of STMN1 and its multiple phosphor-sites in the primary tumor and Kaplan-Meier analysis of DFS in breast cancer patients with high or low STMN1 expression and the expression of its multiple serine phospho-sites A. Representative IHC staining of high and low expression of STMN1 in the large (400×) and small images (100×). B. Representative IHC staining of high and low expression of multiple phosphor-sites (Ser-16, Ser-25, Ser38, Ser63) in the large (400×) and small images (100×). C. Kaplan-Meier analysis of DFS in the training set. D. Kaplan-Meier analysis of DFS in the validation set.

    Journal: Oncotarget

    Article Title: Stathmin and phospho-stathmin protein signature is associated with survival outcomes of breast cancer patients

    doi:

    Figure Lengend Snippet: Identification by immunohistochemistry (IHC) of STMN1 and its multiple phosphor-sites in the primary tumor and Kaplan-Meier analysis of DFS in breast cancer patients with high or low STMN1 expression and the expression of its multiple serine phospho-sites A. Representative IHC staining of high and low expression of STMN1 in the large (400×) and small images (100×). B. Representative IHC staining of high and low expression of multiple phosphor-sites (Ser-16, Ser-25, Ser38, Ser63) in the large (400×) and small images (100×). C. Kaplan-Meier analysis of DFS in the training set. D. Kaplan-Meier analysis of DFS in the validation set.

    Article Snippet: For STMN1 and Ser38, TMAs were blocked with 10% normal goat serum for 1 h at room temperature (RT) and incubated in a humid chamber at 4°C overnight with polyclonal rabbit anti-human STMN1 antibody (Proteintech) or polyclonal rabbit anti-human STMN1 Ser38 (Cell Signaling Technologies) antibody diluted to 1:400 or 1:100, respectively.

    Techniques: Immunohistochemistry, Expressing, Staining