Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Phosphoproteomic Analysis of FLCN Inactivation Highlights Differential Kinase Pathways and Regulatory TFEB Phosphoserines

18 Jul 2022

Abstract excerpt

In Birt–Hogg–Dubé (BHD) syndrome, germline loss-of-function mutations in the Folliculin ( FLCN ) gene lead to an increased risk of renal cancer. To address how FLCN inactivation affects cellular kinase signaling pathways, we analyzed comprehensive phosphoproteomic profiles of FLCN POS and FLCN NEG human renal tubular epithelial cells (RPTEC/TERT1). In total, 15,744 phosphorylated peptides were identified from...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Microtubule and mitosis dynamics
Share to Renal and related cancers
Share to Renal cell carcinoma treatment

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 35863698
DOI: 10.1016/j.mcpro.2022.100263

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Phosphoproteomic Analysis of FLCN Inactivation Highlights Differential Kinase Pathways and Regulatory TFEB PhosphoserinesPMID 35863698Read ↗

Clinical features, genetics and potential therapeutic approaches for Birt–Hogg–Dubé syndromeSemantic proximity Read ↗

Birt-Hogg-Dubé syndrome: from gene discovery to molecularly targeted therapies.Semantic proximity Read ↗

Characterizing the tumor suppressor activity of FLCN in Birt-Hogg-Dubé syndrome cell models through transcriptomic and proteomic analysisSemantic proximity Read ↗

Loss of FLCN-FNIP1/2 induces a non-canonical interferon response in human renal tubular epithelial cellsSemantic proximity Read ↗

Characterizing the tumor suppressor activity of FLCN in Birt-Hogg-Dubé syndrome through transcriptiomic and proteomic analysisSemantic proximity Read ↗

Birt-Hogg-Dubé syndrome: Clinical and molecular aspects of recently identified kidney cancer syndrome.Semantic proximity Read ↗

FLCN: The causative gene for Birt-Hogg-Dubé syndrome.Semantic proximity Read ↗

TFEB and TFE3 drive kidney cystogenesis and tumorigenesisSemantic proximity Read ↗

Evaluation of folliculin detection by immunohistochemistry in Birt-Hogg-Dubé associated kidney tumorsSemantic proximity Read ↗

Birt-Hogg-Dubé renal tumors are genetically distinct from other renal neoplasias and are associated with up-regulation of mitochondrial gene expressionSemantic proximity Read ↗

SQSTM1/p62 accumulation is a hallmark of FLCN loss in Birt-Hogg-Dubé syndrome-associated kidney cancerSemantic proximity Read ↗

Birt-Hogg-Dubé: tumour suppressor function and signalling dynamics central to folliculin.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.