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GAPDH antibody

RRID:AB_2263076

Antibody ID

AB_2263076

Target Antigen

Human GAPD,Recombinant Protein human, rat

Proper Citation

(Proteintech Group Cat# 10494-1-AP, RRID:AB_2263076)

Clonality

polyclonal antibody

Comments

manufacturer recommendations: Immunohistochemistry; Western Blot; ELISA,Western Blot,Immunohistochemistry

Host Organism

rabbit

Vendor

Proteintech Group

Cat Num

10494-1-AP

Publications that use this research resource

SPIN1 promotes tumorigenesis by blocking the uL18 (universal large ribosomal subunit protein 18)-MDM2-p53 pathway in human cancer.

  • Fang Z
  • Elife
  • 2018 Mar 16

Literature context: ch Catalogue number:10494-1-AP; RRID:AB_2263076 Applications: WB


Abstract:

Ribosomal proteins (RPs) play important roles in modulating the MDM2-p53 pathway. However, less is known about the upstream regulators of the RPs. Here, we identify SPIN1 (Spindlin 1) as a novel binding partner of human RPL5/uL18 that is important for this pathway. SPIN1 ablation activates p53, suppresses cell growth, reduces clonogenic ability, and induces apoptosis of human cancer cells. Mechanistically, SPIN1 sequesters uL18 in the nucleolus, preventing it from interacting with MDM2, and thereby alleviating uL18-mediated inhibition of MDM2 ubiquitin ligase activity toward p53. SPIN1 deficiency increases ribosome-free uL18 and uL5 (human RPL11), which are required for SPIN1 depletion-induced p53 activation. Analysis of cancer genomic databases suggests that SPIN1 is highly expressed in several human cancers, and its overexpression is positively correlated with poor prognosis in cancer patients. Altogether, our findings reveal that the oncogenic property of SPIN1 may be attributed to its negative regulation of uL18, leading to p53 inactivation.

Funding information:
  • National Institutes of Health - 2G12MD007595()
  • National Institutes of Health - R01CA095441()
  • National Institutes of Health - R01CA127724()
  • National Institutes of Health - R01CA172468()
  • National Institutes of Health - R21 CA201889()
  • National Institutes of Health - R21CA190775()
  • NCI NIH HHS - CA89194(United States)

Zfp281 is essential for mouse epiblast maturation through transcriptional and epigenetic control of Nodal signaling.

  • Huang X
  • Elife
  • 2017 Nov 23

Literature context: Gapdh (10494-1-AP, ProteinTech, RRID:AB_2263076). Blot intensities were quantif


Abstract:

Pluripotency is defined by a cell's potential to differentiate into any somatic cell type. How pluripotency is transited during embryo implantation, followed by cell lineage specification and establishment of the basic body plan, is poorly understood. Here we report the transcription factor Zfp281 functions in the exit from naive pluripotency occurring coincident with pre-to-post-implantation mouse embryonic development. By characterizing Zfp281 mutant phenotypes and identifying Zfp281 gene targets and protein partners in developing embryos and cultured pluripotent stem cells, we establish critical roles for Zfp281 in activating components of the Nodal signaling pathway and lineage-specific genes. Mechanistically, Zfp281 cooperates with histone acetylation and methylation complexes at target gene enhancers and promoters to exert transcriptional activation and repression, as well as epigenetic control of epiblast maturation leading up to anterior-posterior axis specification. Our study provides a comprehensive molecular model for understanding pluripotent state progressions in vivo during mammalian embryonic development.

Funding information:
  • NIDA NIH HHS - K02 DA021863-01A1(United States)

Systematic Characterization of Autophagy in Gestational Diabetes Mellitus.

  • Ji L
  • Endocrinology
  • 2017 Aug 1

Literature context: AP Rabbit, polyclonal 1:5000 RRID:AB_2263076


Abstract:

Autophagy is a dynamic process that degrades and recycles cellular organelles and proteins to maintain cell homeostasis. Alterations in autophagy occur in various diseases; however, the role of autophagy in gestational diabetes mellitus (GDM) is unknown. In the present study, we characterized the roles and functions of autophagy in GDM patient samples and extravillous trophoblasts cultured with glucose. We found significantly enhanced autophagy in GDM patients. Moreover, high glucose levels enhanced autophagy and cell apoptosis, reducing proliferation and invasion, and these effects were ameliorated through knockdown of ATG5. Genome-wide 5-hydroxymethylcytosine data analysis further revealed the epigenomic regulatory circuitry underlying the induced autophagy and apoptosis in GDM and preeclampsia. Finally, RNA sequencing was performed to identify gene expression changes and critical signaling pathways after silencing of ATG5. Our study has demonstrated the substantial functions of autophagy in GDM and provides potential therapeutic targets for the treatment of GDM patients.

Developmental pattern of the neuronal intermediate filament inaa in the zebrafish retina.

  • Liao ML
  • J. Comp. Neurol.
  • 2016 Dec 15

Literature context: cago, IL, RRID:AB_2263076), and mous


Abstract:

α-Internexin is a member of the neuronal intermediate filament (nIF) protein family, which also includes peripherin and neurofilament (NF) triplet proteins. Previous studies found that expression of α-internexin precedes that of the NF triplet proteins in mammals and suggested that α-internexin plays a key role in the neuronal cytoskeleton network during development. In this study, we aimed to analyze the expression patterns and function of internexin neuronal intermediate filament protein-alpha a (inaa), the encoding gene of which is a homolog of the mammalian α-internexin, during retinal development in zebrafish. Via in vitro and in vivo studies, we demonstrated that zebrafish inaa is an α-internexin homolog that shares characteristics with nIFs. An immunohistochemical analysis of zebrafish revealed that inaa was distributed dynamically in the developing retina. It was widely localized in retinal neuroepithelial cells at 1 day postfertilization (dpf), and was mainly found in the ganglion cell layer (GCL) and inner part of the inner nuclear layer (INL) from 3-9 dpf; after 14 dpf, it was restricted to the outer nuclear layer (ONL). Moreover, we demonstrated for the first time that inaa acted distinctively from the cytoskeletal scaffold of zebrafish cone photoreceptors during development. In conclusion, we demonstrated the morphological features of a novel nIF, inaa, and illustrated its developmental expression pattern in the zebrafish retina. J. Comp. Neurol. 524:3810-3826, 2016. © 2016 Wiley Periodicals, Inc.