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rabbit anti human hhex  (Atlas Antibodies)


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    Atlas Antibodies rabbit anti human hhex
    Figure 1. mRNA and protein expression of <t>HHEX.</t> (A) mRNA expression in controls, multiple sclerosis (MS) patients, and MS patients stratified by treatment. Controls: n = 117; MS patients: n = 154; MS patients treated with IFN-β: n = 94; MS patients treated with glatiramer acetate: n = 57. (B) HHEX mRNA expression in controls and MS patients stratified by rs7923837 genotype. Heterozygotes were grouped with major homozygotes due to similar expression levels. Control GG + GA: n = 101; minor allele homozygous controls AA: n = 16; MS GG + GA: n = 133; MS AA: n = 18; MS GG + GA treated with IFN-β: n = 85; MS AA treated with IFN-β: n = 9; MS GG + GA treated with glatiramer acetate: n = 48; MS AA treated with glatiramer acetate: n = 9. (C) Expression of HHEX protein analyzed by Western blot, stratified by rs7923837 genotype. Control GG + GA: n = 24; Control AA: n = 9; MS GG + GA: n = 36; MS AA: n = 13. Mean and standard deviation are presented in all panels.
    Rabbit Anti Human Hhex, supplied by Atlas Antibodies, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+human+hhex/Anti-HHEX/pm35887298-175-4-8
    Average 93 stars, based on 2 article reviews
    rabbit anti human hhex - by Bioz Stars, 2026-08
    93/100 stars

    Images

    1) Product Images from "Unraveling the Influence of HHEX Risk Polymorphism rs7923837 on Multiple Sclerosis Pathogenesis."

    Article Title: Unraveling the Influence of HHEX Risk Polymorphism rs7923837 on Multiple Sclerosis Pathogenesis.

    Journal: International journal of molecular sciences

    doi: 10.3390/ijms23147956

    Figure 1. mRNA and protein expression of HHEX. (A) mRNA expression in controls, multiple sclerosis (MS) patients, and MS patients stratified by treatment. Controls: n = 117; MS patients: n = 154; MS patients treated with IFN-β: n = 94; MS patients treated with glatiramer acetate: n = 57. (B) HHEX mRNA expression in controls and MS patients stratified by rs7923837 genotype. Heterozygotes were grouped with major homozygotes due to similar expression levels. Control GG + GA: n = 101; minor allele homozygous controls AA: n = 16; MS GG + GA: n = 133; MS AA: n = 18; MS GG + GA treated with IFN-β: n = 85; MS AA treated with IFN-β: n = 9; MS GG + GA treated with glatiramer acetate: n = 48; MS AA treated with glatiramer acetate: n = 9. (C) Expression of HHEX protein analyzed by Western blot, stratified by rs7923837 genotype. Control GG + GA: n = 24; Control AA: n = 9; MS GG + GA: n = 36; MS AA: n = 13. Mean and standard deviation are presented in all panels.
    Figure Legend Snippet: Figure 1. mRNA and protein expression of HHEX. (A) mRNA expression in controls, multiple sclerosis (MS) patients, and MS patients stratified by treatment. Controls: n = 117; MS patients: n = 154; MS patients treated with IFN-β: n = 94; MS patients treated with glatiramer acetate: n = 57. (B) HHEX mRNA expression in controls and MS patients stratified by rs7923837 genotype. Heterozygotes were grouped with major homozygotes due to similar expression levels. Control GG + GA: n = 101; minor allele homozygous controls AA: n = 16; MS GG + GA: n = 133; MS AA: n = 18; MS GG + GA treated with IFN-β: n = 85; MS AA treated with IFN-β: n = 9; MS GG + GA treated with glatiramer acetate: n = 48; MS AA treated with glatiramer acetate: n = 9. (C) Expression of HHEX protein analyzed by Western blot, stratified by rs7923837 genotype. Control GG + GA: n = 24; Control AA: n = 9; MS GG + GA: n = 36; MS AA: n = 13. Mean and standard deviation are presented in all panels.

    Techniques Used: Expressing, Control, Western Blot, Standard Deviation

    Figure 3. Glycolytic profile and mitochondrial mass of PBMCs from multiple sclerosis (MS) patients and controls stratified by the genotypes of HHEX rs7923837. (A) Energy phenotype of the studied groups. Minimum and maximum values of extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) were confronted to obtain an estimation of the metabolic range of the cells. (B–D) Glycolytic analysis comparing carriers of the major allele in HHEX rs7923837 and minor-allele homozygotes from both MS patients and controls. Control GG + GA: n = 11; Control AA: n = 7; MS GG + GA: n = 18; MS AA: n = 7. (E–H) Increase in mitochondrial mass measured by flow cytometry with Mitotracker GreenTM after activation with PHA. The ratio of the median fluorescence intensity in the presence/absence of PHA was calculated for PBMCs (E) and the indicated lymphocyte subpopulations (F–H). Control GG + GA: n = 9; Control AA: n = 5; MS GG + GA: n = 17; MS AA: n = 8. Mean and standard deviation are presented in panels (B–H).
    Figure Legend Snippet: Figure 3. Glycolytic profile and mitochondrial mass of PBMCs from multiple sclerosis (MS) patients and controls stratified by the genotypes of HHEX rs7923837. (A) Energy phenotype of the studied groups. Minimum and maximum values of extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) were confronted to obtain an estimation of the metabolic range of the cells. (B–D) Glycolytic analysis comparing carriers of the major allele in HHEX rs7923837 and minor-allele homozygotes from both MS patients and controls. Control GG + GA: n = 11; Control AA: n = 7; MS GG + GA: n = 18; MS AA: n = 7. (E–H) Increase in mitochondrial mass measured by flow cytometry with Mitotracker GreenTM after activation with PHA. The ratio of the median fluorescence intensity in the presence/absence of PHA was calculated for PBMCs (E) and the indicated lymphocyte subpopulations (F–H). Control GG + GA: n = 9; Control AA: n = 5; MS GG + GA: n = 17; MS AA: n = 8. Mean and standard deviation are presented in panels (B–H).

    Techniques Used: Control, Cytometry, Activation Assay, Standard Deviation



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    Atlas Antibodies rabbit anti human hhex
    Figure 1. mRNA and protein expression of <t>HHEX.</t> (A) mRNA expression in controls, multiple sclerosis (MS) patients, and MS patients stratified by treatment. Controls: n = 117; MS patients: n = 154; MS patients treated with IFN-β: n = 94; MS patients treated with glatiramer acetate: n = 57. (B) HHEX mRNA expression in controls and MS patients stratified by rs7923837 genotype. Heterozygotes were grouped with major homozygotes due to similar expression levels. Control GG + GA: n = 101; minor allele homozygous controls AA: n = 16; MS GG + GA: n = 133; MS AA: n = 18; MS GG + GA treated with IFN-β: n = 85; MS AA treated with IFN-β: n = 9; MS GG + GA treated with glatiramer acetate: n = 48; MS AA treated with glatiramer acetate: n = 9. (C) Expression of HHEX protein analyzed by Western blot, stratified by rs7923837 genotype. Control GG + GA: n = 24; Control AA: n = 9; MS GG + GA: n = 36; MS AA: n = 13. Mean and standard deviation are presented in all panels.
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    Figure 1. mRNA and protein expression of <t>HHEX.</t> (A) mRNA expression in controls, multiple sclerosis (MS) patients, and MS patients stratified by treatment. Controls: n = 117; MS patients: n = 154; MS patients treated with IFN-β: n = 94; MS patients treated with glatiramer acetate: n = 57. (B) HHEX mRNA expression in controls and MS patients stratified by rs7923837 genotype. Heterozygotes were grouped with major homozygotes due to similar expression levels. Control GG + GA: n = 101; minor allele homozygous controls AA: n = 16; MS GG + GA: n = 133; MS AA: n = 18; MS GG + GA treated with IFN-β: n = 85; MS AA treated with IFN-β: n = 9; MS GG + GA treated with glatiramer acetate: n = 48; MS AA treated with glatiramer acetate: n = 9. (C) Expression of HHEX protein analyzed by Western blot, stratified by rs7923837 genotype. Control GG + GA: n = 24; Control AA: n = 9; MS GG + GA: n = 36; MS AA: n = 13. Mean and standard deviation are presented in all panels.
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    Image Search Results


    Figure 1. mRNA and protein expression of HHEX. (A) mRNA expression in controls, multiple sclerosis (MS) patients, and MS patients stratified by treatment. Controls: n = 117; MS patients: n = 154; MS patients treated with IFN-β: n = 94; MS patients treated with glatiramer acetate: n = 57. (B) HHEX mRNA expression in controls and MS patients stratified by rs7923837 genotype. Heterozygotes were grouped with major homozygotes due to similar expression levels. Control GG + GA: n = 101; minor allele homozygous controls AA: n = 16; MS GG + GA: n = 133; MS AA: n = 18; MS GG + GA treated with IFN-β: n = 85; MS AA treated with IFN-β: n = 9; MS GG + GA treated with glatiramer acetate: n = 48; MS AA treated with glatiramer acetate: n = 9. (C) Expression of HHEX protein analyzed by Western blot, stratified by rs7923837 genotype. Control GG + GA: n = 24; Control AA: n = 9; MS GG + GA: n = 36; MS AA: n = 13. Mean and standard deviation are presented in all panels.

    Journal: International journal of molecular sciences

    Article Title: Unraveling the Influence of HHEX Risk Polymorphism rs7923837 on Multiple Sclerosis Pathogenesis.

    doi: 10.3390/ijms23147956

    Figure Lengend Snippet: Figure 1. mRNA and protein expression of HHEX. (A) mRNA expression in controls, multiple sclerosis (MS) patients, and MS patients stratified by treatment. Controls: n = 117; MS patients: n = 154; MS patients treated with IFN-β: n = 94; MS patients treated with glatiramer acetate: n = 57. (B) HHEX mRNA expression in controls and MS patients stratified by rs7923837 genotype. Heterozygotes were grouped with major homozygotes due to similar expression levels. Control GG + GA: n = 101; minor allele homozygous controls AA: n = 16; MS GG + GA: n = 133; MS AA: n = 18; MS GG + GA treated with IFN-β: n = 85; MS AA treated with IFN-β: n = 9; MS GG + GA treated with glatiramer acetate: n = 48; MS AA treated with glatiramer acetate: n = 9. (C) Expression of HHEX protein analyzed by Western blot, stratified by rs7923837 genotype. Control GG + GA: n = 24; Control AA: n = 9; MS GG + GA: n = 36; MS AA: n = 13. Mean and standard deviation are presented in all panels.

    Article Snippet: Cells were stained with rabbit anti-human HHEX (HPA055460, Atlas Antibodies, Bromma, Sweden) as primary antibody, and a combination of biotinylated anti-rabbit antibody (BA-1000, Vector Laboratories, Newark, CA, USA) and streptavidin-Alexa Fluor 555 (S32355, Invitrogen, Waltham, MA, USA) supplemented with Draq5 (ab108410, Abcam, Cambridge, United Kingdom).

    Techniques: Expressing, Control, Western Blot, Standard Deviation

    Figure 3. Glycolytic profile and mitochondrial mass of PBMCs from multiple sclerosis (MS) patients and controls stratified by the genotypes of HHEX rs7923837. (A) Energy phenotype of the studied groups. Minimum and maximum values of extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) were confronted to obtain an estimation of the metabolic range of the cells. (B–D) Glycolytic analysis comparing carriers of the major allele in HHEX rs7923837 and minor-allele homozygotes from both MS patients and controls. Control GG + GA: n = 11; Control AA: n = 7; MS GG + GA: n = 18; MS AA: n = 7. (E–H) Increase in mitochondrial mass measured by flow cytometry with Mitotracker GreenTM after activation with PHA. The ratio of the median fluorescence intensity in the presence/absence of PHA was calculated for PBMCs (E) and the indicated lymphocyte subpopulations (F–H). Control GG + GA: n = 9; Control AA: n = 5; MS GG + GA: n = 17; MS AA: n = 8. Mean and standard deviation are presented in panels (B–H).

    Journal: International journal of molecular sciences

    Article Title: Unraveling the Influence of HHEX Risk Polymorphism rs7923837 on Multiple Sclerosis Pathogenesis.

    doi: 10.3390/ijms23147956

    Figure Lengend Snippet: Figure 3. Glycolytic profile and mitochondrial mass of PBMCs from multiple sclerosis (MS) patients and controls stratified by the genotypes of HHEX rs7923837. (A) Energy phenotype of the studied groups. Minimum and maximum values of extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) were confronted to obtain an estimation of the metabolic range of the cells. (B–D) Glycolytic analysis comparing carriers of the major allele in HHEX rs7923837 and minor-allele homozygotes from both MS patients and controls. Control GG + GA: n = 11; Control AA: n = 7; MS GG + GA: n = 18; MS AA: n = 7. (E–H) Increase in mitochondrial mass measured by flow cytometry with Mitotracker GreenTM after activation with PHA. The ratio of the median fluorescence intensity in the presence/absence of PHA was calculated for PBMCs (E) and the indicated lymphocyte subpopulations (F–H). Control GG + GA: n = 9; Control AA: n = 5; MS GG + GA: n = 17; MS AA: n = 8. Mean and standard deviation are presented in panels (B–H).

    Article Snippet: Cells were stained with rabbit anti-human HHEX (HPA055460, Atlas Antibodies, Bromma, Sweden) as primary antibody, and a combination of biotinylated anti-rabbit antibody (BA-1000, Vector Laboratories, Newark, CA, USA) and streptavidin-Alexa Fluor 555 (S32355, Invitrogen, Waltham, MA, USA) supplemented with Draq5 (ab108410, Abcam, Cambridge, United Kingdom).

    Techniques: Control, Cytometry, Activation Assay, Standard Deviation