PA1-903

antibody from Invitrogen Antibodies

Targeting: CALR cC1qR, CRT, FLJ26680, RO, SSA

Western blot

Immunoprecipitation

Antibody data

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Validation data

Product number: PA1-903 - Provider product page
Provider: Invitrogen Antibodies
Product name: Calreticulin Polyclonal Antibody
Antibody type: Polyclonal
Antigen: Synthetic peptide
Description: PA1-903 detects calreticulin from human, rat, mouse, hamster, rabbit and canine tissues. PA1-903 has been successfully used in Western blot, immunoprecipitation, immunocytochemistry and immunofluorescence procedures. By Western blot, this antibody detects an ~60 kDa protein representing calreticulin and an ~120 kDa unidentified protein from rat brain extract. PA1-903 immunizing peptide corresponds to amino acid residues 399-414 from mouse calreticulin. PA1-903 immunizing peptide (Cat. # PEP-017) is available for use in neutralization and control experiments.
Reactivity: Human, Mouse, Rat, Canine, Hamster, Rabbit
Host: Chicken/Avian
Isotype: IgY
Vial size: 100 μL
Concentration: 1 mg/mL
Storage: -20°C, Avoid Freeze/Thaw Cycles

CALR protein structure - PA1-903 shown in red.

Supportive validation

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig 1 Regional heterogeneity of the insulin-sensitive GLUT4 and GLUT8 in the healthy myocardium. Higher total protein expression of A) GLUT4 and lower B) GLUT8 content in the healthy atrial compared to ventricular myocytes. Top panels: representative Western blot from total lysate of isolated rat myocytes; calsequestrin (CLSQ) was used as a loading control; representative bands were obtained from the same membrane. Bottom panels: Mean +- SE of total GLUT protein content (values expressed relative to atria; n = 6/group); * P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig 2 Analysis of the downstream insulin signaling pathways in the healthy atria. A) Insulin stimulates phosphorylation of Akt at s473 and Th308 site in atrial myocytes. Top panel: representative Western blot from total lysate of isolated rat atrial myocytes incubated with (0.01muM) and without (basal) insulin; calsequestrin (CLSQ) was used as a loading control. Bottom panel: Mean +- SE of protein expression (values expressed relative to basal; n = 5/group); # P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 3 Rapamycin reduces the ER Ca 2+ -leak rate. A-B) Western-blot analysis for luminal Ca 2+ -binding proteins in HeLa cells treated with the indicated concentrations of rapamycin (Rapa) for 5 h: calreticulin (CRT) (A) and BiP/Grp78 (BiP) (B). Upper panels: representative Western blots; lower panels: quantification of the protein/GAPDH ratio ( n = 4). C) Western-blot analysis for SERCA2 in HeLa cells treated with the indicated concentrations of rapamycin for 5 h. Upper panels: representative Western blots; lower panel: quantification of the SERCA2/GAPDH ratio ( n = 4). D) Representative plot showing the decrease in ER 45 Ca 2+ content (logarithmic scale) in a Ca 2+ -free efflux medium without ATP as a function of time in permeabilized HeLa cells pretreated for 5 h with 1 uM rapamycin or with DMSO. The passively bound Ca 2+ was determined by loading the cells with 45 Ca 2+ in the presence of 10 uM of the Ca 2+ ionophore A23187 and then subtracted from the stored 45 Ca 2+ . The ER Ca 2+ -leak rate can be estimated as the rate of decline of the ER 45 Ca 2+ -store content as a function of time. E) Quantification of the mean 45 Ca 2+ -store content at the beginning of the measurement (t 0 ) ( n = 5). F) Quantification of the mean slope of the curve in D after transformation to a linear scale, which is a measure of the 45 Ca 2+ -leak rate ( n = 5). * p

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig 4 Alteration of the trafficking of the insulin-sensitive GLUTs in the diabetic atria. Decreased atrial A) GLUT4 and B) GLUT8 content during type 1 diabetes (T1Dx). Top panels: representative Western blot from crude membrane extract of perfused mouse atria, calsequestrin (CLSQ) was used as a loading control. Bottom panels: Mean +- SE of GLUT protein content (values expressed relative to control; n = 7-8/group). Type 1 diabetes decreased C) GLUT4 and D) GLUT8 trafficking to the atrial cell surface. Top panels: representative Western blot. Bottom panels: Mean +- SE of cell surface GLUT protein content (values expressed relative to control; n = 4-5/group). Majority of E) GLUT4 and F) GLUT8 is intracellular under basal conditions (mean +- SE, values expressed relative to control labeled, n = 5/group). Methods: Intact perfused mouse hearts were photolabeled with bio-LC-ATB-BGPA to determine the amount of cell surface (L: labeled fraction) and intracellular (UL: unlabeled fraction) content. T1Dx: type 1 diabetic; Con: control; * P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig 5 Intact insulin signaling pathway in the atria of insulin-deficient diabetic animals. Type 1 diabetes (T1 Dx) did not alter A) Akt or B) AS160 phosphorylation in the atria . Top panels: representative Western blot from total lysate of mouse atria; calsequestrin (CLSQ) was used as a loading control. Bottom panels: Mean +- SE of protein expression (values expressed relative to control; n = 4-5/group). Insulin stimulates C) GLUT4 and D) GLUT8 trafficking to the atrial cell surface in type 1 diabetic (T1 Dx) subjects . Top panels: representative Western blot. Bottom panels: Mean +- SE of cell surface GLUT protein content (values expressed relative to control basal labeled; n = 4-6/group). Methods: Intact mouse hearts were perfused with and without insulin, and photolabeled with bio-LC-ATB-BGPA to determine the amount of cell surface (L: labeled fraction) and intracellular (UL: unlabeled fraction) content. T1Dx: type 1 diabetic; *P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 3 Alterations in glucose transporter (GLUT) trafficking in the atria of insulin-deficient type 1 diabetic (T1Dx) animals were rescued by in vivo insulin treatment. Total expression of (A) GLUT4 and (B) GLUT8 in the atria of the T1Dx, insulin-treated type 1 diabetic (T1Dx+Insulin), and control (Con) animals. Top panels: representative Western blot from total lysate; loading control: calsequestrin (CLSQ). Bottom Panels: Mean +- SE of total GLUT protein content, normalized to calsequestrin (values normalized to respective controls). Methods: Western blotting. Control: n = 4, T1Dx: n = 3, and T1Dx+Ins: n = 4. Atrial cell surface (C) GLUT4 and (D) GLUT8 protein expression in T1Dx, T1Dx+Insulin, and control animals. Top panels: representative Western blot. Bottom Panels: Mean +- SE of cell surface GLUT protein content (values normalized to controls); Control: n = 4, T1Dx: n = 4, and T1Dx+Ins: n = 5. Methods: biotinylated photolabeling technique in the intact perfused mouse heart. L, Labeled (cell surface fraction); UL, Unlabeled (intracellular fraction). # P < 0.05 vs. Control, * P < 0.05 vs. T1Dx. Statistical test: 1-way ANOVA, two-tailed t -test.