Nagham Theres Asp

• Løchen, Arja Katrina Lea Arnesen; Søreng, Kristiane; Veroni, Chiara; Moncho, Laura Cristina Trachsel; Asp, Nagham Theres & Gaupset, Robin [Vis alle 10 forfattere av denne artikkelen] (2026). Interaction of HS1BP3 with cortactin modulates TKS5 localisation, cell secretion and cancer malignancy. Molecular Oncology. ISSN 1574-7891. doi: 10.1002/1878-0261.70248. Fulltekst i vitenarkiv Vis sammendrag

  The HCLS1-Binding Protein 3 (HS1BP3) interacts with the SH3 domain of cortactin (CTTN), a protein that contributes to a malignant phenotype in cancers. Here, we demonstrate that high expression of HS1BP3 is associated with reduced survival for gastric adenocarcinoma and triple negative breast carcinoma patients and that HS1BP3 is specifically upregulated in these cancers. We mapped the HS1BP3-cortactin interaction site to the third proline-rich region (PRR3.1) of HS1BP3 and show that this interaction is important for cancer cell proliferation, extracellular matrix degradation and secretion. HS1BP3 expression was found to correlate with expression of the invadopodia scaffold protein TKS5 and we show that the localisation of TKS5 inside multivesicular endosomes is increased in cells expressing an HS1BP3 PRR3.1 mutant. Overall, our results highlight the importance of the direct interaction between HS1BP3 and cortactin in cancer development by regulating cell proliferation, secretion and invasion, which may provide an explanation for the negative correlation between HS1BP3 levels and the survival of gastric adenocarcinoma and triple negative breast cancer patients.

• Moncho, Laura Cristina Trachsel; Veroni, Chiara; Mathai, Benan John; Lapao, Ana Sofia Da Silva; Singh, Sakshi & Asp, Nagham Theres [Vis alle 9 forfattere av denne artikkelen] (2025). SNX10 functions as a modulator of piecemeal mitophagy and mitochondrial bioenergetics. Journal of Cell Biology. ISSN 0021-9525. 224(5). doi: 10.1083/jcb.202404009. Fulltekst i vitenarkiv Vis sammendrag

  We here identify the endosomal protein SNX10 as a negative regulator of piecemeal mitophagy of OXPHOS machinery components. In control conditions, SNX10 localizes to early endocytic compartments in a PtdIns3P-dependent manner and modulates endosomal trafficking but also shows dynamic connections with mitochondria. Upon hypoxia-mimicking conditions, SNX10 localizes to late endosomal structures containing selected mitochondrial proteins, including COX-IV and SAMM50, and the autophagy proteins SQSTM1/p62 and LC3B. The turnover of COX-IV was enhanced in SNX10-depleted cells, with a corresponding reduced mitochondrial respiration and citrate synthase activity. Importantly, zebrafish larvae lacking Snx10 show reduced levels of Cox-IV, as well as elevated ROS levels and ROS-mediated cell death in the brain, demonstrating the in vivo relevance of SNX10-mediated modulation of mitochondrial bioenergetics.

• Sharma, Kulbhushan; Asp, Nagham Theres; Harrison, Sean; Siller, Richard; Baumgarten, Saphira Felicitas & Gupta, Swapnil [Vis alle 10 forfattere av denne artikkelen] (2021). Autophagy modulates cell fate decisions during lineage commitment. Autophagy. ISSN 1554-8627. s. 1–17. doi: 10.1080/15548627.2021.2008691. Fulltekst i vitenarkiv Vis sammendrag

  Early events during development leading to exit from a pluripotent state and commitment toward a specific germ layer still need in depth understanding. Autophagy has been shown to play a crucial role in both development and differentiation. This study employs human embryonic and induced pluripotent stem cells to understand the early events of lineage commitment with respect to the role of autophagy in this process. Our data indicate that a dip in autophagy facilitates exit from pluripotency. Upon exit, we demonstrate that the modulation of autophagy affects SOX2 levels and lineage commitment, with induction of autophagy promoting SOX2 degradation and mesendoderm formation, whereas inhibition of autophagy causes SOX2 accumulation and neuroectoderm formation. Thus, our results indicate that autophagy-mediated SOX2 turnover is a determining factor for lineage commitment. These findings will deepen our understanding of development and lead to improved methods to derive different lineages and cell types.

• Asp, Nagham Theres; Kvalvaag, Audun Sverre Myrset; Sandvig, Kirsten & Pust, Sascha (2016). Regulation of ErbB2 localization and function in breast cancer cells by ERM proteins. OncoTarget. 7(18), s. 25443–25460. doi: 10.18632/oncotarget.8327. Fulltekst i vitenarkiv
• Asp, Nagham; Pust, Sascha & Sandvig, Kirsten (2014). Flotillin depletion affects ErbB protein levels in different human breast cancer cells. BBA - Molecular Cell Research. ISSN 0167-4889. 1843(9), s. 1987–1996. doi: 10.1016/j.bbamcr.2014.04.013. Fulltekst i vitenarkiv
• Pust, Sascha; Klokk, Tove Irene; Musa, Nagham; Jenstad, Monica; Risberg, Bjørn Åke & Erikstein, Bjørn K [Vis alle 11 forfattere av denne artikkelen] (2013). Flotillins as regulators of ErbB2 levels in breast cancer. Oncogene. ISSN 0950-9232. 32(29), s. 3443–3451. doi: 10.1038/onc.2012.357. Fulltekst i vitenarkiv

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