PA1-845

antibody from Invitrogen Antibodies

Targeting: NCOA3 ACTR, AIB1, bHLHe42, CAGH16, KAT13B, p/CIP, RAC3, SRC-3, SRC3, TNRC16, TRAM-1

Provider product page for PA1-845

Western blot

Other assay

Antibody data

Antibody Data
Antigen structure
References [12]
Comments [0]
Validations
Other assay [11]

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Product number: PA1-845 - Provider product page
Provider: Invitrogen Antibodies
Product name: SRC3 Polyclonal Antibody
Antibody type: Polyclonal
Antigen: Synthetic peptide
Description: PA1-845 detects amplified in breast cancer 1 (AIB1) from human tissues and cells. PA1-845 has been successfully used in Western blot procedures. By Western blot, this antibody detects an ~155 kDa protein representing AIB1 from T47D cell lysate. The PA1-845 immunogen is a synthetic peptide corresponding to residues G(3) L G E N L D P L A S D S(15) C of human AIB1. PA1-845 can be used with blocking peptide PEP-049.
Reactivity: Human
Host: Rabbit
Isotype: IgG
Vial size: 100 µg
Concentration: 1 mg/mL
Storage: -20°C, Avoid Freeze/Thaw Cycles

NCOA3 protein structure - PA1-845 shown in red.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 1 UPR preconditioning renders the hTERT-HM uterine myocyte CASP3 non-apoptotic. a Elevated levels of cytoplasmic GRP78 and Cl CASP3, and nuclear Cl PARP are observed in preconditioned (P) and non-preconditioned (NP) uterine myocytes as compared to controls (C) ( n = 3 per condition), when exposed to a cytotoxic dose of TM 0, 4, 24, and 48 h post TM preconditioning. At 48 h to recovery there is equal activation of GRP78 ( b ) and Cl CASP3 ( c ) in both P and NP uterine myocytes. In contrast, Cl PARP ( d ) is significantly decreased in the P versus NP cells. PDIA2 and NCOA3 are utilized as cytoplasmic and nuclear protein loading controls. A representative blot from this experiment is shown. Statistical comparisons were performed using one-way ANOVA, and subsequent Newman-Keuls multiple-comparison tests. Data labeled with different letters are significantly different from each other ( p < 0.05)

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 2 UPR preconditioning ablates NF-kappaB activation in the hTERT-HM uterine myocyte. a , b , d , e Activation of NF-kappaB was significantly increased in both TM and Thaps non-preconditioned (NP) cells and reduced to barely detectable levels in preconditioned (P) cells 2 h post administration of a cytotoxic dose of TM/Thaps. c , f TNFalpha secretion was also reduced in P versus NP cells. A representative blot from each experiment is shown. NCOA3 is utilized as nuclear protein loading control. Statistical comparisons were performed using one-way ANOVA, and subsequent Newman-Keuls multiple-comparison tests. Data labeled with different letters are significantly different from each other ( p < 0.05)

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 3 UPR preconditioning differentially regulates activation of the pro and anti-apoptotic arms of the UPR in the hTERT-HM uterine myocyte. TM ( a ) or Thaps ( f ) mediated preconditioning blocked activation of the pro-apoptotic arms of the UPR with ATF4 ( d , i ) and GADD153 ( e , j ) and TM preconditioning maintained activation of the anti-apoptotic arm of the UPR with XBP1s ( c ) significantly upregulated in preconditioned (P) versus non-preconditioned (NP) cells post administration of a cytotoxic dose of TM/Thaps. No changes in XBP1s ( h ) upon Thaps treatment, and p-eIF2alpha ( b , g ) upon TM and Thaps treatment. PDIA2 and NCOA3 are utilized as cytoplasmic and nuclear protein loading controls. A representative blot from each experiment is shown. Statistical comparisons were performed using one-way ANOVA, and subsequent Newman-Keuls multiple-comparison tests. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared with controls

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 5 Endogenous preconditioning facilitates the maintenance of non-apoptotic CASP3 and suppresses iPLA2 activation in the pregnant mouse uterus. Uteri collected from vehicle treated (Con), sub-preconditioned (PBA), exogenously stressed-sub-preconditioned (TM+PBA) and exogenously stressed-preconditioned (TM) mice on E17 prior to the onset of preterm and term birth were examined for a active Cl CASP3. b Cl PARP, and c TUNEL staining to measure apoptotic cell death. iPLA2t levels act as an indirect measure of iPLA2 activation ( d ). Cl CASP3 levels remained unchanged across all 4 groups examined however increased Cl PARP and TUNEL activity and decreased levels of the inactive iPLA2t were isolated to the TM+PBA-treated mice. e In the hTERT-HM cells the cleaved active monomeric form of iPLA2 (iPLA2cm) was elevated in a relative manner to the levels of apoptotic CASP3 present in the preconditioned and non-preconditioned cells (Fig. 1a ). A representative blot or image from each experiment is shown. PDIA2 and NCOA3 are utilized as cytoplasmic and nuclear protein loading controls. Statistical comparisons were performed using one-way ANOVA, and subsequent Newman-Keuls multiple-comparison tests. Data labeled with different letters are significantly different from each other ( p < 0.05)

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 5 Gestational regulation of ER stress signaling in the pregnant mouse uterus from E6-E19. A) Analysis of protein expression of DDIT3 and XBP1(S) in the nuclear fraction of a gestational series of mouse uteri from E6-19. NCOA3 was used as a loading control. Graphs of ROD of B) DDIT3 and C) XBP1(S) normalized to NCOA3. D) Representative western blots of cleaved (CL) and full length (FL) CASP12 in the cytoplasmic fraction across gestation. PDI was used as a loading control. ROD of E) CL CASP12 and F) FL CASP12 normalized to PDI. Data are represented as Mean ROD +- SE. N = 3 for each time point. Data labeled with different letters are significantly different from each other (P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 5 hnRNPG expression declines in myometrium from women at term. Representative western blot (A) and densitometric analysis (B) demonstrates a significant decline in hnRNPG protein levels in nuclear extracts of term laboring (TL) and term non-laboring (TNL) myometrium compared to myometrium from preterm non-laboring (PTNL) women. Q-PCR analysis (C) also demonstrates a significant decline in hnRNPG TNL myometrium compared to myometrium from PTNL women. Representative western blot (D) and densitometric analysis demonstrating a significant decline in hnRNPG (E) and ERDelta7 (F) protein levels upon estradiol (E2) treatment in the hTERT-HM cell. hTERT-HM cells were treated with vehicle, progesterone (100 nM; P4) or E2 (100 nM) for 24 h. Nuclear extracts were prepared and analyzed for hnRNPG and ERDelta7 proteins. NCOA3 is used as nuclear loading control. Gene expression was normalized to Rplp0 . *p < 0.05 using one-way ANOVA, followed by the Newman-Keuls multiple-comparison test; each experiment was performed in triplicate with n = 4 per group. Data shown are mean +- SEM. Fig. 5