anti-Peripherin (PRPH) Antibodies

Human Peripherin (PRPH) interaction partners

1. Desmin (show DES Antibodies), Glial Fibrillary Acidic Protein (show GFAP Antibodies), Vimentin (show VIM Antibodies), and Peripherin are type III intermediate filaments that have roles in health and disease [review]

2. To discover of Phosphorylated autoantigens Peripherin as a Major Humoral Autoantigen in Type 1 Diabetes Mellitus.

3. In patients with HD, a panel using calretinin and peripherin with or without MAP-2 may be most helpful in identifying transition zones

4. interaction between disease-causing RAB7A (show RAB7A Antibodies) mutants and peripherin could play an important role in Charcot-Marie-Tooth type 2B neuropathy

5. This work contributes to determine the role of PRPH gene variants in ALS. Further studies are necessary to define the mechanisms through which the mutant peripherin could cause ALS phenotype.

6. study analyzed expression of peripherin(PP) in the cochlea; in organ of Corti, PP seems to be specifically expressed in outer hair cell afferents; small or type II spiral ganglion cell bodies also intensely express PP

7. although the mechanisms underlying peripherin co-localization in Bunina bodies are unknown, peripherin could be involved in forming these inclusions

8. Transgenic peripherin isoform expression reveals post-transcriptional changes to the normal expression pattern associated with malformed filaments and intracellular inclusions underlying a role in the pathogenesis of amyotrophic lateral sclerosis.

9. The data of this experiment document the expression of peripherin in Lewy body-like inclusions , which may provide a clue to the pathogenesis of neurodegeneration in ALS.

10. Peripherin overexpression in transgenic mice can cause defective transport of type IV neurofilament proteins, a phenomenon that may account for the progressive formation of amyotrophic lateral sclerosis-like spheroids in axons.

Mouse (Murine) Peripherin (PRPH) interaction partners

1. Data suggest that the underlying molecular mechanisms in amyotrophic lateral sclerosis pathogenesis involve peripherin mis (show AMH Antibodies)-splicing and altered homeostasis of nerve fibers.

2. Contralateral and ipsilateral olivocochlear efferent-mediated suppression of the cochlear amplifier were absent in Prph null mice.

3. Data suggest anti-peripherin (PRPH) B cells represent a heterogeneous population that is generated early in life but proliferates as diabetes is established.

4. peripherin appears to be a participant in learning and memory impairment in mice

5. rather than forming an independent structure, peripherin is a subunit of neurofilaments in the adult peripheral nervous system

6. Peripherin isoform expression and inclusion formation serve a physiologically relevant role in the pathology of amyotrophic lateral sclerosis.

7. Complex post-transcriptional processes may underlie the continuum between peripherin-mediated neuronal repair and its pathogenic role in a transgenic model of amyotrophic lateral sclerosis.

8. Peripherin may interact with other cytoskeletal elements to regulate outgrowth of the peripheral neurites of type II SGN, distinguishing these neurons from the type I SGN innervating the inner hair cells.

9. peripherin gene sequences direct Cre recombinase (show RAG1 Antibodies) expression to peripheral neurons in transgenic mice.

10. Overexpression of peripherin in mice deficient for neurofilament light (NF-L (show NEFL Antibodies)) subunits induced a progressive ALS-like spinal motor neuron degeneration (show CLN8 Antibodies) prevented by simultaneous overexpression of NF-H (show NEFH Antibodies)