Synapsin I in PC12 cells. I. Characterization of the phosphoprotein and effect of chronic NGF treatment.

نویسندگان

  • C Romano
  • R A Nichols
  • P Greengard
  • L A Greene
چکیده

PC12 cells contain a synapsin I-like molecule. Several serum and monoclonal antibodies raised against bovine brain synapsin I bind to and precipitate this molecule, demonstrating immunochemical similarity between the brain and PC12 species. PC12 synapsin I, like brain synapsin I, is a phosphoprotein: It is phosphorylated in intact cells and, when partially purified, serves as a substrate for several synapsin I kinases. PC12 cell synapsin I is structurally similar to brain synapsin I as shown by peptide mapping of 35S-methionine-and 32P-phosphate-labeled molecules from the 2 sources. Chronic NGF treatment of the cells induces a significant increase in the amount of synapsin I relative to total cell protein, measured either by immunolabeling or incorporation of 35S-methionine. The synapsin I present in untreated PC12 cells migrates predominantly as a singlet and that present in cells treated chronically with NGF as a doublet in SDS-PAGE.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Induction of Bone Marrow Stromal Cells into Cholinergic-Like Cells by Nerve Growth Factor

Background: Bone marrow stromal cells (BMSC) are used as a source for cell therapy in different model for neurological disorder such as stroke and spinal cord injury. However, the transdifferentiation of BMSC into cholinergic phenotype requires more investigation. Methods: BMSC were isolated from adult rats, pre-induced with β-mercaptoethanol (BME) and followed by nerve growth factor (NGF) indu...

متن کامل

Protective effect of Nigella sativa and thymoquinone on serum/glucose deprivation-induced DNA damage in PC12 cells

Objective: The discovery and development of natural products with potent antioxidant properties has been one of the most interesting and promising approaches in the search for treatment of CNS injuries. The most significant consequence of the oxidative stress is thought to be the DNA modifications, which can become permanent via the formation of mutations and other types of genomic instability ...

متن کامل

Co-expression of recombinant human nerve growth factor with trigger factor chaperone in E. coli

Nerve growth factor (NGF) is a neurotrophic factor that is functional in the survival, maintenance and differentiation of nervous system cells. This protein has three subunits, of which the beta subunit has the main activity. Its structure consists of a cysteine knot motif made up of beta strands linked by disulfide bonds. It can be used as a therapeutic agent in the treatment of many diseases....

متن کامل

Nerve growth factor inhibits PC12 cell PDE 2 phosphodiesterase activity and increases PDE 2 binding to phosphoproteins.

Nerve growth factor (NGF) has been shown to increase cyclic AMP in PC12 cells and to potentiate the actions of other agents that raise cyclic AMP. In our studies, NGF causes over 50% loss of PDE 2 activity (cyclic GMP-stimulated cyclic nucleotide phosphodiesterase) in PC12 cells within 24 h. After 72 h of NGF treatment, cyclic AMP hydrolysis in PC12 extracts is no longer cyclic GMP-stimulated. ...

متن کامل

Mitochondrial Complex I Is an Essential Player in LPS-Induced Preconditioning in Differentiated PC12 Cells

Preconditioning (PC) as a protective strategy against noxious insults can decline cell death and apoptosis. It has been approved that mitochondria play a key role in PC mechanism. The critical role of complex I (CI) in oxidative phosphorylation machinery and intracellular ROS production, particularly in the brain, accentuates its possible role in PC-induced neuroprotection. Here, differentiated...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • The Journal of neuroscience : the official journal of the Society for Neuroscience

دوره 7 5  شماره 

صفحات  -

تاریخ انتشار 1987