- PA1-845 - Invitrogen Antibodies NCOA3 antibody

Submitted references Estrogen receptor alpha isoform ERdelta7 in myometrium modulates uterine quiescence during pregnancy.

Anamthathmakula P, Kyathanahalli C, Ingles J, Hassan SS, Condon JC, Jeyasuria P
EBioMedicine 2019 Jan;39:520-530

Preconditioning the uterine unfolded protein response maintains non-apoptotic Caspase 3-dependent quiescence during pregnancy.

Ingles J, Simpson A, Kyathanahalli C, Anamthathmakula P, Hassan S, Jeyasuria P, Condon JC
Cell death & disease 2018 Sep 17;9(10):933

The Unfolded Protein Response Regulates Uterine Myocyte Antioxidant Responsiveness During Pregnancy.

Ramnarayanan S, Kyathanahalli C, Ingles J, Park-York M, Jeyasuria P, Condon JC
Biology of reproduction 2016 Dec;95(6):120

Uterine endoplasmic reticulum stress-unfolded protein response regulation of gestational length is caspase-3 and -7-dependent.

Kyathanahalli C, Organ K, Moreci RS, Anamthathmakula P, Hassan SS, Caritis SN, Jeyasuria P, Condon JC
Proceedings of the National Academy of Sciences of the United States of America 2015 Nov 10;112(45):14090-5

Uterine endoplasmic reticulum stress and its unfolded protein response may regulate caspase 3 activation in the pregnant mouse uterus.

Suresh A, Subedi K, Kyathanahalli C, Jeyasuria P, Condon JC
PloS one 2013;8(9):e75152

Research resource: identification of novel coregulators specific for thyroid hormone receptor-β2.

Hahm JB, Privalsky ML
Molecular endocrinology (Baltimore, Md.) 2013 May;27(5):840-59

Cross-species withdrawal of MCL1 facilitates postpartum uterine involution in both the mouse and baboon.

Kyathanahalli C, Marks J, Nye K, Lao B, Albrecht ED, Aberdeen GW, Nathanielsz PW, Jeyasuria P, Condon JC
Endocrinology 2013 Dec;154(12):4873-84

Antiapoptotic signaling via MCL1 confers resistance to caspase-3-mediated apoptotic cell death in the pregnant human uterine myocyte.

Stephenson-Famy A, Marks J, Suresh A, Caritis SN, Simhan H, Jeyasuria P, Condon JC
Molecular endocrinology (Baltimore, Md.) 2012 Feb;26(2):320-30

Electromagnetic fields alter the expression of estrogen receptor cofactors in breast cancer cells.

Girgert R, Gründker C, Emons G, Hanf V
Bioelectromagnetics 2008 Apr;29(3):169-76

Histone acetylation in keratinocytes enables control of the expression of cathelicidin and CD14 by 1,25-dihydroxyvitamin D3.

Schauber J, Oda Y, Büchau AS, Yun QC, Steinmeyer A, Zügel U, Bikle DD, Gallo RL
The Journal of investigative dermatology 2008 Apr;128(4):816-24

Development and therapeutic options for the treatment of raloxifene-stimulated breast cancer in athymic mice.

O'Regan RM, Osipo C, Ariazi E, Lee ES, Meeke K, Morris C, Bertucci A, Sarker MA, Grigg R, Jordan VC
Clinical cancer research : an official journal of the American Association for Cancer Research 2006 Apr 1;12(7 Pt 1):2255-63

Factor recruitment and TIF2/GRIP1 corepressor activity at a collagenase-3 response element that mediates regulation by phorbol esters and hormones.

Rogatsky I, Zarember KA, Yamamoto KR
The EMBO journal 2001 Nov 1;20(21):6071-83

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Western blot of human AIB1 in T47D cell lysate using Product # PA1-845.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Western blot of human AIB1 in T47D cell lysate using Product # PA1-845.

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: 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)
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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)
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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

PA1-845

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