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Goat Anti-PTBP1 Polyclonal Antibody, Unconjugated


Antibody ID


Target Antigen

PTBP1 human, rat, reacts with human and rat (see review)not yet tested in other speciespredicted to react with mouse due to sequence homology

Proper Citation

(Abcam Cat# ab5642, RRID:AB_305011)


polyclonal antibody


validation status unknown, seller recommendations provided in 2012: Immunoprecipitation; Western Blot; Immunoprecipitation, Western Blot

Host Organism




Cat Num


Publications that use this research resource

PTBP1-Mediated Alternative Splicing Regulates the Inflammatory Secretome and the Pro-tumorigenic Effects of Senescent Cells.

  • Georgilis A
  • Cancer Cell
  • 2018 Jul 9

Literature context:


Oncogene-induced senescence is a potent tumor-suppressive response. Paradoxically, senescence also induces an inflammatory secretome that promotes carcinogenesis and age-related pathologies. Consequently, the senescence-associated secretory phenotype (SASP) is a potential therapeutic target. Here, we describe an RNAi screen for SASP regulators. We identified 50 druggable targets whose knockdown suppresses the inflammatory secretome and differentially affects other SASP components. Among the screen candidates was PTBP1. PTBP1 regulates the alternative splicing of genes involved in intracellular trafficking, such as EXOC7, to control the SASP. Inhibition of PTBP1 prevents the pro-tumorigenic effects of the SASP and impairs immune surveillance without increasing the risk of tumorigenesis. In conclusion, our study identifies SASP inhibition as a powerful and safe therapy against inflammation-driven cancer.

Funding information:
  • Wellcome Trust - U117588499(88499)(United Kingdom)

Cell-Type-Specific Alternative Splicing Governs Cell Fate in the Developing Cerebral Cortex.

  • Zhang X
  • Cell
  • 2016 Aug 25

Literature context:


Alternative splicing is prevalent in the mammalian brain. To interrogate the functional role of alternative splicing in neural development, we analyzed purified neural progenitor cells (NPCs) and neurons from developing cerebral cortices, revealing hundreds of differentially spliced exons that preferentially alter key protein domains-especially in cytoskeletal proteins-and can harbor disease-causing mutations. We show that Ptbp1 and Rbfox proteins antagonistically govern the NPC-to-neuron transition by regulating neuron-specific exons. Whereas Ptbp1 maintains apical progenitors partly through suppressing a poison exon of Flna in NPCs, Rbfox proteins promote neuronal differentiation by switching Ninein from a centrosomal splice form in NPCs to a non-centrosomal isoform in neurons. We further uncover an intronic human mutation within a PTBP1-binding site that disrupts normal skipping of the FLNA poison exon in NPCs and causes a brain-specific malformation. Our study indicates that dynamic control of alternative splicing governs cell fate in cerebral cortical development.