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

Hypothyroid phenotype is contributed by mitochondrial complex I inactivation due to translocated neuronal nitric-oxide synthase.

The Journal of biological chemistry - 24 Feb 2006

Franco María C, Antico Arciuch Valeria G, Peralta Jorge G, Galli Soledad, Levisman Damián, López Lidia M, Romorini Leonardo, Poderoso Juan J, Carreras María C

Abstract excerpt

Although transcriptional effects of thyroid hormones have substantial influence on oxidative metabolism, how thyroid sets basal metabolic rate remains obscure. Compartmental localization of nitric-oxide synthases is important for nitric oxide signaling. We therefore examined liver neuronal nitric-oxide synthase-alpha (nNOS) subcellular distribution as a putative mechanism for thyroid effects on rat metabolic...

Read the complete abstract on PubMed

Topics

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

Share to Electrons
Share to Hypothyroidism

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Microscopy, Immunoelectron

Share to Mitochondria, Liver

Share to NG-Nitroarginine Methyl Ester

Share to Nitric Oxide Synthase Type I

Share to Oxidants

Share to Thyroid Hormones

Source

Identifiers

PMID: 16361261
DOI: 10.1074/jbc.M512080200

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Hypothyroid phenotype is contributed by mitochondrial complex I inactivation due to translocated neuronal nitric-oxide synthase.PMID 16361261Read ↗

High fat diet induces dysregulation of hepatic oxygen gradients and mitochondrial functionin vivoSemantic proximity Read ↗

Mitochondrial and energetic cardiac phenotype in hypothyroid rat. Relevance to heart failure.Semantic proximity Read ↗

Exogenous Thyroxine Increases Cardiac Nrf2-TRX Associated with a Reduction in Oxidative Injury and Inflammation in Insulin Resistant OLETF RatsSemantic proximity Read ↗

Beyond T3: The Emerging Role of 3,5-Diiodothyronine in Mitochondrial Thyroid Hormone SignalingSemantic proximity Read ↗

Dysregulation of Nitrosylation Dynamics Promotes Nitrosative Stress and Contributes to Cardiometabolic Heart Failure with Preserved Ejection FractionSemantic proximity Read ↗

The modulation of mitochondrial nitric-oxide synthase activity in rat brain development.Semantic proximity Read ↗

S-nitrosylated GAPDH initiates apoptotic cell death by nuclear translocation following Siah1 binding.Semantic proximity Read ↗

Central Hypothyroidism Impairs Heart Rate Stability and Prevents Thyroid Hormone-Induced Cardiac Hypertrophy and Pyrexia.Semantic proximity Read ↗

The role of nitric oxide in muscle fibers with oxidative phosphorylation defects.Semantic proximity Read ↗

Thyroid hormone transporters in health and disease: advances in thyroid hormone deiodination.Semantic proximity Read ↗

GSNOR Deficiency Enhances In Situ Skeletal Muscle Strength, Fatigue Resistance, and RyR1 S-Nitrosylation Without Impacting Mitochondrial Content and Activity.Semantic proximity Read ↗

Chronic inorganic nitrate supplementation does not improve metabolic health and worsens disease progression in mice with diet-induced obesitySemantic proximity Read ↗

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