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Unbiased label-free quantitative proteomics of Amyotrophic lateral sclerosis (ALS) mutations in CCNF reveals activation of the apoptosis pathway

ABSTRACT: The past 10 years has seen a rapid acceleration in the discovery of new genetic causes of ALS, with more than 20 putative ALS-causing genes now cited. These genes express proteins that cover a diverse range of molecular functions, including free radical scavenging (cf SOD1), regulation of RNA homeostasis (cf TDP-43, FUS), and protein degradation through the ubiquitin-proteasome system (cf ubiquilin-2, Cyclin F) and autophagy. However, not all of the reported ALS-causing genes have been replicated in subsequent genetic studies – raising significant question marks on the true validity of some putative ALS genes (such as profilin and angiogenin). Furthermore, it still remains unclear what common molecular mechanisms or pathways link these diverse genes/proteins, such that defects in these individual proteins ultimately converge to cause ALS. This study seeks to develop an innovative pipeline to start to address some of these questions.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Neuronal Stem Cell

DISEASE(S): Frontotemporal Dementia,Amyotrophic Lateral Sclerosis

SUBMITTER: Albert Lee

LAB HEAD: Albert Lee

PROVIDER: PXD021793 | Pride | 2021-03-31

REPOSITORIES: Pride

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			Action	DRS
	180403_CCNF_EMP_R1_01.raw	Raw
	180403_CCNF_EMP_R1_02.raw	Raw
	180403_CCNF_EMP_R1_03.raw	Raw
	180403_CCNF_EMP_R1_04.raw	Raw
	180403_CCNF_EMP_R1_05.raw	Raw

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Unbiased label-free quantitative proteomics of Amyotrophic lateral sclerosis (ALS) mutations in CCNF reveals activation of the apoptosis pathway

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