Pabpn1 cDNA ORF clone, Mus musculus(house mouse)

Novel mouse models of oculopharyngeal muscular dystrophy (OPMD) reveal early onset mitochondrial defects and suggest loss of PABPN1 may contribute to pathology.
Vest KE, Phillips BL, Banerjee A, Apponi LH, Dammer EB, Xu W, Zheng D, Yu J, Tian B, Pavlath GK, Corbett AH
Human molecular genetics26(17)3235-3252(2017 Sep)

Functional impact of an oculopharyngeal muscular dystrophy mutation in PABPN1.
Garc?a-Casta?eda M, Vega AV, Rodr?guez R, Montiel-Jaen MG, Cisneros B, Zarain-Herzberg A, Avila G
The Journal of physiology595(13)4167-4187(2017 Jul)

Cytokine genes as potential biomarkers for muscle weakness in OPMD.
Riaz M, Raz Y, van der Slujis B, Dickson G, van Engelen B, Vissing J, Raz V
Human molecular genetics25(19)4282-4287(2016 10)

A genome-wide in situ hybridization map of RNA-binding proteins reveals anatomically restricted expression in the developing mouse brain.
McKee AE, Minet E, Stern C, Riahi S, Stiles CD, Silver PA
BMC developmental biology514(2005 Jul)

Matrin 3 (MATR3) is a novel protein interactor of PABPN1. MATR3 also binds and regulates the levels of long non-coding RNA (lncRNA) Neat1 and together with PABPN1 is required for normal paraspeckle function.
Title: Nuclear poly(A) binding protein 1 (PABPN1) and Matrin3 interact in muscle cells and regulate RNA processing.

Expression levels of these cytokines were highly correlated in controls, but this correlation pattern was disrupted in OPMD. The levels of these 6 cytokines were not altered in expPABPN1 carriers at a pre-symptomatic stage, suggesting that this group of cytokines is a potential biomarker for muscle weakness in OPMD.
Title: Cytokine genes as potential biomarkers for muscle weakness in OPMD.

educed PABPN1 levels caused a consistent decline in distal PAS utilization in the 3'-UTR of a subset of OPMD-dysregulated genes. This alternative PAS utilization led to up-regulation of Atrogin-1, a key muscle atrophy regulator, but down regulation of proteasomal genes. Additionally reduced PABPN1 levels caused a reduction in proteasomal activity, and transition in MyHC isotope expression pattern in myofibers.
Title: PABPN1-Dependent mRNA Processing Induces Muscle Wasting.

These findings demonstrate a role for PABPN1 in rescuing several cytopathological features of TDP-43 proteinopathy by increasing the turnover of pathologic proteins.
Title: PABPN1 suppresses TDP-43 toxicity in ALS disease models.

PABPN1 interacts with and is stabilized by heat shock protein 90.
Title: The Inhibition of Heat Shock Protein 90 Facilitates the Degradation of Poly-Alanine Expanded Poly (A) Binding Protein Nuclear 1 via the Carboxyl Terminus of Heat Shock Protein 70-Interacting Protein.