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polyclonal anti alc1 antibody  (Boster Bio)


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    Boster Bio polyclonal anti alc1 antibody
    Fig. 1. Isolation of <t>ALC1</t> from 1q21 amplicon. (A) Amplification of different regions along chromosome 1q in 60 HCC cases was detected by FISH. The number of cases amplified is indicated above each bar. (B) FISH analysis showed that the amplified microdissected DNA probe was specifically hybridized to normal chromosome 1q21 (red signals). This microdissected DNA was used for cDNA selection from an HCC case with 1q21 amplification. (C) ALC1 was mapped to 1q21 by FISH with a BAC clone containing ALC1 (indicated by arrows). (D) A representative exam- ple of ALC1 gene amplification detected in H-4 cells by FISH with the BAC probe (red signals). A BAC probe from 1p32 (green signals) was used as a control. (E) ALC1 was cloned to pEGFP vector. The exogenously expressed ALC1-EGFP fusion protein (green color) was sublocalized in the nucleus. (F) Compared to CHD1, the predicted protein structure of ALC1 also has SNF2_N and HELICc domains.
    Polyclonal Anti Alc1 Antibody, supplied by Boster Bio, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/polyclonal anti alc1 antibody/product/Boster Bio
    Average 86 stars, based on 1 article reviews
    polyclonal anti alc1 antibody - by Bioz Stars, 2026-04
    86/100 stars

    Images

    1) Product Images from "Isolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma."

    Article Title: Isolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma.

    Journal: Hepatology (Baltimore, Md.)

    doi: 10.1002/hep.22072

    Fig. 1. Isolation of ALC1 from 1q21 amplicon. (A) Amplification of different regions along chromosome 1q in 60 HCC cases was detected by FISH. The number of cases amplified is indicated above each bar. (B) FISH analysis showed that the amplified microdissected DNA probe was specifically hybridized to normal chromosome 1q21 (red signals). This microdissected DNA was used for cDNA selection from an HCC case with 1q21 amplification. (C) ALC1 was mapped to 1q21 by FISH with a BAC clone containing ALC1 (indicated by arrows). (D) A representative exam- ple of ALC1 gene amplification detected in H-4 cells by FISH with the BAC probe (red signals). A BAC probe from 1p32 (green signals) was used as a control. (E) ALC1 was cloned to pEGFP vector. The exogenously expressed ALC1-EGFP fusion protein (green color) was sublocalized in the nucleus. (F) Compared to CHD1, the predicted protein structure of ALC1 also has SNF2_N and HELICc domains.
    Figure Legend Snippet: Fig. 1. Isolation of ALC1 from 1q21 amplicon. (A) Amplification of different regions along chromosome 1q in 60 HCC cases was detected by FISH. The number of cases amplified is indicated above each bar. (B) FISH analysis showed that the amplified microdissected DNA probe was specifically hybridized to normal chromosome 1q21 (red signals). This microdissected DNA was used for cDNA selection from an HCC case with 1q21 amplification. (C) ALC1 was mapped to 1q21 by FISH with a BAC clone containing ALC1 (indicated by arrows). (D) A representative exam- ple of ALC1 gene amplification detected in H-4 cells by FISH with the BAC probe (red signals). A BAC probe from 1p32 (green signals) was used as a control. (E) ALC1 was cloned to pEGFP vector. The exogenously expressed ALC1-EGFP fusion protein (green color) was sublocalized in the nucleus. (F) Compared to CHD1, the predicted protein structure of ALC1 also has SNF2_N and HELICc domains.

    Techniques Used: Isolation, Amplification, Selection, Control, Clone Assay, Plasmid Preparation

    Fig. 2. Overexpression of ALC1 in primary HCCs and HCC cell lines. (A) A representative example of ALC1 amplification in HCC TMA detected by FISH with the BAC clone contain- ing ALC1. (B) A 98-kD protein was detected by anti-ALC1 antibody. (C) Positive nuclear staining of ALC1 was frequently detected in primary HCC (left) but not in its matched adjacent nontumor tissue specimen (right) by IHC. (D) The IHC result in TMA was verified on a larger tissue section containing HCC tissue (upper part) and surrounding nontumor liver tissue (lower part). RNA expression of ALC1 was tested in (E) primary HCC cases and(F) HCC cell lines by north- ern blot analysis. In primary HCC, ALC1 expression was compared be- tween tumors (T) and their matched nontumor liver tissues (N).
    Figure Legend Snippet: Fig. 2. Overexpression of ALC1 in primary HCCs and HCC cell lines. (A) A representative example of ALC1 amplification in HCC TMA detected by FISH with the BAC clone contain- ing ALC1. (B) A 98-kD protein was detected by anti-ALC1 antibody. (C) Positive nuclear staining of ALC1 was frequently detected in primary HCC (left) but not in its matched adjacent nontumor tissue specimen (right) by IHC. (D) The IHC result in TMA was verified on a larger tissue section containing HCC tissue (upper part) and surrounding nontumor liver tissue (lower part). RNA expression of ALC1 was tested in (E) primary HCC cases and(F) HCC cell lines by north- ern blot analysis. In primary HCC, ALC1 expression was compared be- tween tumors (T) and their matched nontumor liver tissues (N).

    Techniques Used: Over Expression, Staining, RNA Expression, Expressing

    Fig. 3. Oncogenic ability of ALC1. (A) Expression of ALC1 in ALC1- transfected LO2 and QGY-7703 cells detected by northern blot hybrid- ization. Blank vector–transfected cells were used as controls. (B) Rates of colony formation in soft agar detected in ALC1-transfected and blank vector–transfected LO2 and QGY-7703 cells (**P 0.05). (C,D) Rep- resentative examples of tumors formed in nude mice following injection of ALC1-expressing LO2 cells (left) and QGY-7703 cells (right). ALC1- expressing cells and mock cells were injected into the right and left dorsal flanks, respectively. (E) Flow cytometry histogram showing that overex- pression of ALC1 in ALC1-expressing QGY-7703 cells could promote G1/S phase transition compared to vector-transfected QGY-7703 cells.
    Figure Legend Snippet: Fig. 3. Oncogenic ability of ALC1. (A) Expression of ALC1 in ALC1- transfected LO2 and QGY-7703 cells detected by northern blot hybrid- ization. Blank vector–transfected cells were used as controls. (B) Rates of colony formation in soft agar detected in ALC1-transfected and blank vector–transfected LO2 and QGY-7703 cells (**P 0.05). (C,D) Rep- resentative examples of tumors formed in nude mice following injection of ALC1-expressing LO2 cells (left) and QGY-7703 cells (right). ALC1- expressing cells and mock cells were injected into the right and left dorsal flanks, respectively. (E) Flow cytometry histogram showing that overex- pression of ALC1 in ALC1-expressing QGY-7703 cells could promote G1/S phase transition compared to vector-transfected QGY-7703 cells.

    Techniques Used: Expressing, Transfection, Northern Blot, Plasmid Preparation, Injection, Flow Cytometry, Sublimation

    Fig. 4. Silencing ALC1 expression by siRNA. (A) Two siRNAs (ALC1-si1 and ALC1-si2) could efficiently reduce the expression of ALC1 in H2-M cells. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) served as an internal control. (B) Colony formation ability in soft agar was decreased significantly in siRNA-treated H2-M cells (**P 0.05). (C) Flow cytometry analysis showed that ALC1-si1 could inhibit the cell cycle at the G1/S checkpoint. The percentage of cells in the S phase was decreased from 35% to 23.7%. (D) Western blot analyses indicated that p53 and p21Waf1/Cip1 were down-regulated, whereas cyclin E and Cdk2 were up-regulated in ALC1-transfected QGY-7703 cells in comparison with vector-transfected QGY-7703 cells. -Actin was used as a loading control. (E) Western blot results were quantified by densitometry, and data are presented as mean standard error (n 3). Fold values were first normalized with actin and then compared with vector-transfected QGY-7703 cells.
    Figure Legend Snippet: Fig. 4. Silencing ALC1 expression by siRNA. (A) Two siRNAs (ALC1-si1 and ALC1-si2) could efficiently reduce the expression of ALC1 in H2-M cells. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) served as an internal control. (B) Colony formation ability in soft agar was decreased significantly in siRNA-treated H2-M cells (**P 0.05). (C) Flow cytometry analysis showed that ALC1-si1 could inhibit the cell cycle at the G1/S checkpoint. The percentage of cells in the S phase was decreased from 35% to 23.7%. (D) Western blot analyses indicated that p53 and p21Waf1/Cip1 were down-regulated, whereas cyclin E and Cdk2 were up-regulated in ALC1-transfected QGY-7703 cells in comparison with vector-transfected QGY-7703 cells. -Actin was used as a loading control. (E) Western blot results were quantified by densitometry, and data are presented as mean standard error (n 3). Fold values were first normalized with actin and then compared with vector-transfected QGY-7703 cells.

    Techniques Used: Expressing, Control, Flow Cytometry, Western Blot, Transfection, Comparison, Plasmid Preparation

    Fig. 5. The inhibition role of ALC1 in apoptosis. (A) Representative figures of TUNEL staining images. After cells were treated with STS for 4 hours, more apoptotic cells (bright white) were detected in vector- transfected QGY-7703 cells in comparison with ALC1-transfected 7703 cells. (B) Detection of the apoptotic index between ALC1-transfected and vector-transfected QGY-7703 cells before and after STS treatment (**P 0.05). The data showed that ALC1-transfected QGY-7703 cells could resist STS-induced apoptosis in comparison with QGY-7703 only. (C) Expressions of caspase 3 and Bax were compared between ALC1- transfected and vector-transfected QGY-7703 cells before and after STS treatment by western blot analyses. -Actin was used as a loading control. (D) Protein levels of caspase 3 and Bax were quantified by densitometry, and data are shown as mean standard error (n 3).
    Figure Legend Snippet: Fig. 5. The inhibition role of ALC1 in apoptosis. (A) Representative figures of TUNEL staining images. After cells were treated with STS for 4 hours, more apoptotic cells (bright white) were detected in vector- transfected QGY-7703 cells in comparison with ALC1-transfected 7703 cells. (B) Detection of the apoptotic index between ALC1-transfected and vector-transfected QGY-7703 cells before and after STS treatment (**P 0.05). The data showed that ALC1-transfected QGY-7703 cells could resist STS-induced apoptosis in comparison with QGY-7703 only. (C) Expressions of caspase 3 and Bax were compared between ALC1- transfected and vector-transfected QGY-7703 cells before and after STS treatment by western blot analyses. -Actin was used as a loading control. (D) Protein levels of caspase 3 and Bax were quantified by densitometry, and data are shown as mean standard error (n 3).

    Techniques Used: Inhibition, TUNEL Assay, Staining, Plasmid Preparation, Transfection, Comparison, Western Blot, Control



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    polyclonal anti alc1 antibody  (Boster Bio)
    86
    Boster Bio polyclonal anti alc1 antibody
    Fig. 1. Isolation of <t>ALC1</t> from 1q21 amplicon. (A) Amplification of different regions along chromosome 1q in 60 HCC cases was detected by FISH. The number of cases amplified is indicated above each bar. (B) FISH analysis showed that the amplified microdissected DNA probe was specifically hybridized to normal chromosome 1q21 (red signals). This microdissected DNA was used for cDNA selection from an HCC case with 1q21 amplification. (C) ALC1 was mapped to 1q21 by FISH with a BAC clone containing ALC1 (indicated by arrows). (D) A representative exam- ple of ALC1 gene amplification detected in H-4 cells by FISH with the BAC probe (red signals). A BAC probe from 1p32 (green signals) was used as a control. (E) ALC1 was cloned to pEGFP vector. The exogenously expressed ALC1-EGFP fusion protein (green color) was sublocalized in the nucleus. (F) Compared to CHD1, the predicted protein structure of ALC1 also has SNF2_N and HELICc domains.
    Polyclonal Anti Alc1 Antibody, supplied by Boster Bio, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/polyclonal anti alc1 antibody/product/Boster Bio
    Average 86 stars, based on 1 article reviews
    polyclonal anti alc1 antibody - by Bioz Stars, 2026-04
    86/100 stars
    		  Buy from Supplier

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    Fig. 1. Isolation of ALC1 from 1q21 amplicon. (A) Amplification of different regions along chromosome 1q in 60 HCC cases was detected by FISH. The number of cases amplified is indicated above each bar. (B) FISH analysis showed that the amplified microdissected DNA probe was specifically hybridized to normal chromosome 1q21 (red signals). This microdissected DNA was used for cDNA selection from an HCC case with 1q21 amplification. (C) ALC1 was mapped to 1q21 by FISH with a BAC clone containing ALC1 (indicated by arrows). (D) A representative exam- ple of ALC1 gene amplification detected in H-4 cells by FISH with the BAC probe (red signals). A BAC probe from 1p32 (green signals) was used as a control. (E) ALC1 was cloned to pEGFP vector. The exogenously expressed ALC1-EGFP fusion protein (green color) was sublocalized in the nucleus. (F) Compared to CHD1, the predicted protein structure of ALC1 also has SNF2_N and HELICc domains.

    Journal: Hepatology (Baltimore, Md.)

    Article Title: Isolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma.

    doi: 10.1002/hep.22072

    Figure Lengend Snippet: Fig. 1. Isolation of ALC1 from 1q21 amplicon. (A) Amplification of different regions along chromosome 1q in 60 HCC cases was detected by FISH. The number of cases amplified is indicated above each bar. (B) FISH analysis showed that the amplified microdissected DNA probe was specifically hybridized to normal chromosome 1q21 (red signals). This microdissected DNA was used for cDNA selection from an HCC case with 1q21 amplification. (C) ALC1 was mapped to 1q21 by FISH with a BAC clone containing ALC1 (indicated by arrows). (D) A representative exam- ple of ALC1 gene amplification detected in H-4 cells by FISH with the BAC probe (red signals). A BAC probe from 1p32 (green signals) was used as a control. (E) ALC1 was cloned to pEGFP vector. The exogenously expressed ALC1-EGFP fusion protein (green color) was sublocalized in the nucleus. (F) Compared to CHD1, the predicted protein structure of ALC1 also has SNF2_N and HELICc domains.

    Article Snippet: TMA sections were deparaffinized and incubated with polyclonal anti-ALC1 antibody (Boster Biotechnology Co., Ltd., Wuhan, China) in a dilution of 1:100 at 4°C overnight.

    Techniques: Isolation, Amplification, Selection, Control, Clone Assay, Plasmid Preparation

    Fig. 2. Overexpression of ALC1 in primary HCCs and HCC cell lines. (A) A representative example of ALC1 amplification in HCC TMA detected by FISH with the BAC clone contain- ing ALC1. (B) A 98-kD protein was detected by anti-ALC1 antibody. (C) Positive nuclear staining of ALC1 was frequently detected in primary HCC (left) but not in its matched adjacent nontumor tissue specimen (right) by IHC. (D) The IHC result in TMA was verified on a larger tissue section containing HCC tissue (upper part) and surrounding nontumor liver tissue (lower part). RNA expression of ALC1 was tested in (E) primary HCC cases and(F) HCC cell lines by north- ern blot analysis. In primary HCC, ALC1 expression was compared be- tween tumors (T) and their matched nontumor liver tissues (N).

    Journal: Hepatology (Baltimore, Md.)

    Article Title: Isolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma.

    doi: 10.1002/hep.22072

    Figure Lengend Snippet: Fig. 2. Overexpression of ALC1 in primary HCCs and HCC cell lines. (A) A representative example of ALC1 amplification in HCC TMA detected by FISH with the BAC clone contain- ing ALC1. (B) A 98-kD protein was detected by anti-ALC1 antibody. (C) Positive nuclear staining of ALC1 was frequently detected in primary HCC (left) but not in its matched adjacent nontumor tissue specimen (right) by IHC. (D) The IHC result in TMA was verified on a larger tissue section containing HCC tissue (upper part) and surrounding nontumor liver tissue (lower part). RNA expression of ALC1 was tested in (E) primary HCC cases and(F) HCC cell lines by north- ern blot analysis. In primary HCC, ALC1 expression was compared be- tween tumors (T) and their matched nontumor liver tissues (N).

    Article Snippet: TMA sections were deparaffinized and incubated with polyclonal anti-ALC1 antibody (Boster Biotechnology Co., Ltd., Wuhan, China) in a dilution of 1:100 at 4°C overnight.

    Techniques: Over Expression, Staining, RNA Expression, Expressing

    Fig. 3. Oncogenic ability of ALC1. (A) Expression of ALC1 in ALC1- transfected LO2 and QGY-7703 cells detected by northern blot hybrid- ization. Blank vector–transfected cells were used as controls. (B) Rates of colony formation in soft agar detected in ALC1-transfected and blank vector–transfected LO2 and QGY-7703 cells (**P 0.05). (C,D) Rep- resentative examples of tumors formed in nude mice following injection of ALC1-expressing LO2 cells (left) and QGY-7703 cells (right). ALC1- expressing cells and mock cells were injected into the right and left dorsal flanks, respectively. (E) Flow cytometry histogram showing that overex- pression of ALC1 in ALC1-expressing QGY-7703 cells could promote G1/S phase transition compared to vector-transfected QGY-7703 cells.

    Journal: Hepatology (Baltimore, Md.)

    Article Title: Isolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma.

    doi: 10.1002/hep.22072

    Figure Lengend Snippet: Fig. 3. Oncogenic ability of ALC1. (A) Expression of ALC1 in ALC1- transfected LO2 and QGY-7703 cells detected by northern blot hybrid- ization. Blank vector–transfected cells were used as controls. (B) Rates of colony formation in soft agar detected in ALC1-transfected and blank vector–transfected LO2 and QGY-7703 cells (**P 0.05). (C,D) Rep- resentative examples of tumors formed in nude mice following injection of ALC1-expressing LO2 cells (left) and QGY-7703 cells (right). ALC1- expressing cells and mock cells were injected into the right and left dorsal flanks, respectively. (E) Flow cytometry histogram showing that overex- pression of ALC1 in ALC1-expressing QGY-7703 cells could promote G1/S phase transition compared to vector-transfected QGY-7703 cells.

    Article Snippet: TMA sections were deparaffinized and incubated with polyclonal anti-ALC1 antibody (Boster Biotechnology Co., Ltd., Wuhan, China) in a dilution of 1:100 at 4°C overnight.

    Techniques: Expressing, Transfection, Northern Blot, Plasmid Preparation, Injection, Flow Cytometry, Sublimation

    Fig. 4. Silencing ALC1 expression by siRNA. (A) Two siRNAs (ALC1-si1 and ALC1-si2) could efficiently reduce the expression of ALC1 in H2-M cells. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) served as an internal control. (B) Colony formation ability in soft agar was decreased significantly in siRNA-treated H2-M cells (**P 0.05). (C) Flow cytometry analysis showed that ALC1-si1 could inhibit the cell cycle at the G1/S checkpoint. The percentage of cells in the S phase was decreased from 35% to 23.7%. (D) Western blot analyses indicated that p53 and p21Waf1/Cip1 were down-regulated, whereas cyclin E and Cdk2 were up-regulated in ALC1-transfected QGY-7703 cells in comparison with vector-transfected QGY-7703 cells. -Actin was used as a loading control. (E) Western blot results were quantified by densitometry, and data are presented as mean standard error (n 3). Fold values were first normalized with actin and then compared with vector-transfected QGY-7703 cells.

    Journal: Hepatology (Baltimore, Md.)

    Article Title: Isolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma.

    doi: 10.1002/hep.22072

    Figure Lengend Snippet: Fig. 4. Silencing ALC1 expression by siRNA. (A) Two siRNAs (ALC1-si1 and ALC1-si2) could efficiently reduce the expression of ALC1 in H2-M cells. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) served as an internal control. (B) Colony formation ability in soft agar was decreased significantly in siRNA-treated H2-M cells (**P 0.05). (C) Flow cytometry analysis showed that ALC1-si1 could inhibit the cell cycle at the G1/S checkpoint. The percentage of cells in the S phase was decreased from 35% to 23.7%. (D) Western blot analyses indicated that p53 and p21Waf1/Cip1 were down-regulated, whereas cyclin E and Cdk2 were up-regulated in ALC1-transfected QGY-7703 cells in comparison with vector-transfected QGY-7703 cells. -Actin was used as a loading control. (E) Western blot results were quantified by densitometry, and data are presented as mean standard error (n 3). Fold values were first normalized with actin and then compared with vector-transfected QGY-7703 cells.

    Article Snippet: TMA sections were deparaffinized and incubated with polyclonal anti-ALC1 antibody (Boster Biotechnology Co., Ltd., Wuhan, China) in a dilution of 1:100 at 4°C overnight.

    Techniques: Expressing, Control, Flow Cytometry, Western Blot, Transfection, Comparison, Plasmid Preparation

    Fig. 5. The inhibition role of ALC1 in apoptosis. (A) Representative figures of TUNEL staining images. After cells were treated with STS for 4 hours, more apoptotic cells (bright white) were detected in vector- transfected QGY-7703 cells in comparison with ALC1-transfected 7703 cells. (B) Detection of the apoptotic index between ALC1-transfected and vector-transfected QGY-7703 cells before and after STS treatment (**P 0.05). The data showed that ALC1-transfected QGY-7703 cells could resist STS-induced apoptosis in comparison with QGY-7703 only. (C) Expressions of caspase 3 and Bax were compared between ALC1- transfected and vector-transfected QGY-7703 cells before and after STS treatment by western blot analyses. -Actin was used as a loading control. (D) Protein levels of caspase 3 and Bax were quantified by densitometry, and data are shown as mean standard error (n 3).

    Journal: Hepatology (Baltimore, Md.)

    Article Title: Isolation and characterization of a novel oncogene, amplified in liver cancer 1, within a commonly amplified region at 1q21 in hepatocellular carcinoma.

    doi: 10.1002/hep.22072

    Figure Lengend Snippet: Fig. 5. The inhibition role of ALC1 in apoptosis. (A) Representative figures of TUNEL staining images. After cells were treated with STS for 4 hours, more apoptotic cells (bright white) were detected in vector- transfected QGY-7703 cells in comparison with ALC1-transfected 7703 cells. (B) Detection of the apoptotic index between ALC1-transfected and vector-transfected QGY-7703 cells before and after STS treatment (**P 0.05). The data showed that ALC1-transfected QGY-7703 cells could resist STS-induced apoptosis in comparison with QGY-7703 only. (C) Expressions of caspase 3 and Bax were compared between ALC1- transfected and vector-transfected QGY-7703 cells before and after STS treatment by western blot analyses. -Actin was used as a loading control. (D) Protein levels of caspase 3 and Bax were quantified by densitometry, and data are shown as mean standard error (n 3).

    Article Snippet: TMA sections were deparaffinized and incubated with polyclonal anti-ALC1 antibody (Boster Biotechnology Co., Ltd., Wuhan, China) in a dilution of 1:100 at 4°C overnight.

    Techniques: Inhibition, TUNEL Assay, Staining, Plasmid Preparation, Transfection, Comparison, Western Blot, Control