38 kDa BFA-dependent ADP-ribosylation substrate, aging associated gene 9 protein, Aging-associated gene 9 protein, BARS-38, cb609, EC 1.2.1.12, Epididymis secretory sperm binding protein Li 162eP, G3PD, G3PDH, G3P_HUMAN, GAPD, Glyceraldehyde 3 phosphate dehydrogenase, Glyceraldehyde-3-phosphate dehydrogenase, HEL S 162eP, HEL-S-162eP, KNC-NDS6, MGC102544, MGC102546, MGC103190, MGC103191, MGC105239, MGC127711, MGC88685, OCAS, p38 component, OCT1 coactivator in S phase, 38-KD component, peptidyl cysteine S nitrosylase GAPDH, Peptidyl-cysteine S-nitrosylase GAPDH, wu:fb33a10

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Goat IgG (A121671)

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Dichiarazione di non responsabilità

Questo prodotto è solo per uso di ricerca. Non è inteso per uso diagnostico o terapeutico.

Immagini (2)

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Figure 1: Western Blot - Anti-GAPDH Antibody (A121592)

HMEC-1, Hepa 1-6, and U-118 cell lysates detected with Anti-GADPH Antibody at a 1:1,000 dilution. Lysates at 100µg per lane and rabbit anti-goat IgG antibody (HRP) at a 1:10,000 dilution.

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Figure 2: Anti-GAPDH Antibody (A121592)

Hepa 1-6 cells, fixed with methanol, stained with Anti-GAPDH Antibody at a 1:50 dilution.

Pubblicazioni (6)

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Peptidyl-Prolyl Isomerase 1 Regulates Ca²⁺ Handling by Modulating Sarco(Endo)Plasmic Reticulum Calcium ATPase and Na²⁺/Ca²⁺ Exchanger 1 Protein Levels and Function.

Riferimenti: Anti-GAPDH Antibody (A121592)

Astratto:

BACKGROUND:

Aberrant Ca²⁺ handling is a prominent feature of heart failure. Elucidation of the molecular mechanisms responsible for aberrant Ca²⁺ handling is essential for the development of strategies to blunt pathological changes in calcium dynamics. The peptidyl-prolyl cis-trans isomerase peptidyl-prolyl isomerase 1 (Pin1) is a critical mediator of myocardial hypertrophy development and cardiac progenitor cell cycle. However, the influence of Pin1 on calcium cycling regulation has not been explored. On the basis of these findings, the aim of this study is to define Pin1 as a novel modulator of Ca²⁺ handling, with implications for improving myocardial contractility and potential for ameliorating development of heart failure.

METHODS AND RESULTS:

Pin1 gene deletion or pharmacological inhibition delays cytosolic Ca²⁺ decay in isolated cardiomyocytes. Paradoxically, reduced Pin1 activity correlates with increased sarco(endo)plasmic reticulum calcium ATPase (SERCA2a) and Na²⁺/Ca²⁺ exchanger 1 protein levels. However, SERCA2a ATPase activity and calcium reuptake were reduced in sarcoplasmic reticulum membranes isolated from Pin1-deficient hearts, suggesting that Pin1 influences SERCA2a function. SERCA2a and Na²⁺/Ca²⁺ exchanger 1 associated with Pin1, as revealed by proximity ligation assay in myocardial tissue sections, indicating that regulation of Ca²⁺ handling within cardiomyocytes is likely influenced through Pin1 interaction with SERCA2a and Na²⁺/Ca²⁺ exchanger 1 proteins.

CONCLUSIONS:

Pin1 serves as a modulator of SERCA2a and Na²⁺/Ca²⁺ exchanger 1 Ca²⁺ handling proteins, with loss of function resulting in impaired cardiomyocyte relaxation, setting the stage for subsequent investigations to assess Pin1 dysregulation and modulation in the progression of heart failure.

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(2)

Empowering human cardiac progenitor cells by P2Y₁₄ nucleotide receptor overexpression.

Riferimenti: Anti-GAPDH Antibody (A121592)

Astratto:

KEY POINTS:

Autologous cardiac progenitor cell (CPC) therapy is a promising approach for treatment of heart failure (HF). There is an unmet need to identify inherent deficits in aged/diseased human CPCs (hCPCs) derived from HF patients in the attempts to augment their regenerative capacity prior to use in the clinical setting. Here we report significant functional correlations between phenotypic properties of hCPCs isolated from cardiac biopsies of HF patients, clinical parameters of patients and expression of the P2Y₁₄ purinergic receptor (P2Y₁₄ R), a crucial detector for extracellular UDP-sugars released during injury/stress. P2Y₁₄ R is downregulated in hCPCs derived from HF patients with lower ejection fraction or diagnosed with diabetes. Augmenting P2Y₁₄ R expression levels in aged/diseased hCPCs antagonizes senescence and improves functional responses. This study introduces purinergic signalling modulation as a potential strategy to rejuvenate and improve phenotypic characteristics of aged/functionally compromised hCPCs prior to transplantation in HF patients.

ABSTRACT:

Autologous cardiac progenitor cell therapy is a promising alternative approach to current inefficient therapies for heart failure (HF). However, ex vivo expansion and pharmacological/genetic modification of human cardiac progenitor cells (hCPCs) are necessary interventions to rejuvenate aged/diseased cells and improve their regenerative capacities. This study was designed to assess the potential of improving hCPC functional capacity by targeting the P2Y₁₄ purinergic receptor (P2Y₁₄ R), which has been previously reported to induce regenerative and anti-senescence responses in a variety of experimental models. c-Kit⁺ hCPCs were isolated from cardiac biopsies of multiple HF patients undergoing left ventricular assist device implantation surgery. Significant correlations existed between the expression of P2Y₁₄ R in hCPCs and clinical parameters of HF patients. P2Y₁₄ R was downregulated in hCPCs derived from patients with a relatively lower ejection fraction and patients diagnosed with diabetes. hCPC lines with lower P2Y₁₄ R expression did not respond to P2Y₁₄ R agonist UDP-glucose (UDP-Glu) while hCPCs with higher P2Y₁₄ R expression showed enhanced proliferation in response to UDP-Glu stimulation. Mechanistically, UDP-Glu stimulation enhanced the activation of canonical growth signalling pathways ERK1/2 and AKT. Restoring P2Y₁₄ R expression levels in functionally compromised hCPCs via lentiviral-mediated overexpression improved proliferation, migration and survival under stress stimuli. Additionally, P2Y₁₄ R overexpression reversed senescence-associated morphology and reduced levels of molecular markers of senescence p16^INK4a , p53, p21 and mitochondrial reactive oxygen species. Findings from this study unveil novel biological roles of the UDP-sugar receptor P2Y₁₄ in hCPCs and suggest purinergic signalling modulation as a promising strategy to improve phenotypic properties of functionally impaired hCPCs.

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Protective Effect of a GLP-1 Analog on Ischemia-Reperfusion Induced Blood-Retinal Barrier Breakdown and Inflammation.

Riferimenti: Anti-GAPDH Antibody (A121592)

Astratto:

PURPOSE:

Inflammation associated with blood-retinal barrier (BRB) breakdown is a common feature of several retinal diseases. Therefore, the development of novel nonsteroidal anti-inflammatory approaches may provide important therapeutic options. Previous studies demonstrated that inhibition of dipeptidyl peptidase-IV, the enzyme responsible for the degradation of glucagon-like peptide-1 (GLP-1), led to insulin-independent prevention of diabetes-induced increases in BRB permeability, suggesting that incretin-based drugs may have beneficial pleiotropic effects in the retina. In the current study, the barrier protective and anti-inflammatory properties of exendin-4 (Ex-4), an analog of GLP-1, after ischemia-reperfusion (IR) injury were examined.

METHODS:

Ischemia-reperfusion injury was induced in rat retinas by increasing the intraocular pressure for 45 minutes followed by 48 hours of reperfusion. Rats were treated with Ex-4 prior to and following IR. Blood-retinal barrier permeability was assessed by Evans blue dye leakage. Retinal inflammatory gene expression and leukocytic infiltration were measured by qRT-PCR and immunofluorescence, respectively. A microglial cell line was used to determine the effects of Ex-4 on lipopolysaccharide (LPS)-induced inflammatory response.

RESULTS:

Exendin-4 dramatically reduced the BRB permeability induced by IR injury, which was associated with suppression of inflammatory gene expression. Moreover, in vitro studies showed that Ex-4 also reduced the inflammatory response to LPS and inhibited NF-?B activation.

CONCLUSIONS:

The present work suggests that Ex-4 can prevent IR injury-induced BRB breakdown and inflammation through inhibition of inflammatory cytokine production by activated microglia and may provide a novel option for therapeutic intervention in diseases involving retinal inflammation.

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Hypoxia Prevents Mitochondrial Dysfunction and Senescence in Human c-Kit⁺ Cardiac Progenitor Cells.

Riferimenti: Anti-GAPDH Antibody (A121592)

Astratto:

Senescence-associated dysfunction deleteriously affects biological activities of human c-Kit⁺ cardiac progenitor cells (hCPCs), particularly under conditions of in vitro culture. In comparison, preservation of self-renewal and decreases in mitochondrial reactive oxygen species (ROS) are characteristics of murine CPCs in vivo that reside within hypoxic niches. Recapitulating hypoxic niche oxygen tension conditions of ~1% O₂ in vitro for expansion of hCPCs rather than typical normoxic cell culture conditions (21% O₂ ) could provide significant improvement of functional and biological activities of hCPCs. hCPCs were isolated and expanded under permanent hypoxic (hCPC-1%) or normoxic (hCPC-21%) conditions from left ventricular tissue explants collected during left ventricular assist device implantation. hCPC-1% exhibit increased self-renewal and suppression of senescence characteristics relative to hCPC-21%. Oxidative stress contributed to higher susceptibility to apoptosis, as well as decreased mitochondrial function in hCPC-21%. Hypoxia prevented accumulation of dysfunctional mitochondria, supporting higher oxygen consumption rates and mitochondrial membrane potential. Mitochondrial ROS was an upstream mediator of senescence since treatment of hCPC-1% with mitochondrial inhibitor antimycin A recapitulated mitochondrial dysfunction and senescence observed in hCPC-21%. NAD⁺ /NADH ratio and autophagic flux, which are key factors for mitochondrial function, were higher in hCPC-1%, but hCPC-21% were highly dependent on BNIP3/NIX-mediated mitophagy to maintain mitochondrial function. Overall, results demonstrate that supraphysiological oxygen tension during in vitro expansion initiates a downward spiral of oxidative stress, mitochondrial dysfunction, and cellular energy imbalance culminating in early proliferation arrest of hCPCs. Senescence is inhibited by preventing ROS through hypoxic culture of hCPCs. Stem Cells 2019;37:555-567.

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RAL-1 controls multivesicular body biogenesis and exosome secretion.

Riferimenti: Anti-GAPDH Antibody (A121592)

Astratto:

Exosomes are secreted vesicles arising from the fusion of multivesicular bodies (MVBs) with the plasma membrane. Despite their importance in various processes, the molecular mechanisms controlling their formation and release remain unclear. Using nematodes and mammary tumor cells, we show that Ral GTPases are involved in exosome biogenesis. In Caenorhabditis elegans, RAL-1 localizes at the surface of secretory MVBs. A quantitative electron microscopy analysis of RAL-1-deficient animals revealed that RAL-1 is involved in both MVB formation and their fusion with the plasma membrane. These functions do not involve the exocyst complex, a common Ral guanosine triphosphatase (GTPase) effector. Furthermore, we show that the target membrane SNARE protein SYX-5 colocalizes with a constitutively active form of RAL-1 at the plasma membrane, and MVBs accumulate under the plasma membrane when SYX-5 is absent. In mammals, RalA and RalB are both required for the secretion of exosome-like vesicles in cultured cells. Therefore, Ral GTPases represent new regulators of MVB formation and exosome release.

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CiteAb: a searchable antibody database that ranks antibodies by the number of times they have been cited.

Riferimenti: Anti-GAPDH Antibody (A121592)

Astratto:

BACKGROUND:

Research antibodies are used by thousands of scientists working in diverse disciplines, but it is common to hear concerns about antibody quality. This means that researchers need to carefully choose the antibodies they use to avoid wasting time and money. A well accepted way of selecting a research antibody is to identify one which has been used previously, where the associated data has been peer-reviewed and the results published.

DESCRIPTION:

CiteAb is a searchable database which ranks antibodies by the number of times they have been cited. This allows researchers to easily find antibodies that have been used in peer-reviewed publications and the accompanying citations are listed, so users can check the data contained within the publications. This makes CiteAb a useful resource for identifying antibodies for experiments and also for finding information to demonstrate antibody validation. The database currently contains 1,400,000 antibodies which are from 90 suppliers, including 87 commercial companies and 3 academic resources. Associated with these antibodies are 140,000 publications which provide 306,000 antibody citations. In addition to searching, users can also browse through the antibodies and add their own publications to the CiteAb database.

CONCLUSIONS:

CiteAb provides a new way for researchers to find research antibodies that have been used successfully in peer-reviewed publications. It aims to assist these researchers and will hopefully help promote progress in many areas of life science research.

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