Paper3972829
The ATP dependence of the degradation of short- and long-lived proteins in growing fibroblasts.
Gronostajski RM and 2 others. J Biol Chem, 1985. Cited by 103 papers, by iCite.
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ConductScience Library. The ATP dependence of the degradation of short- and long-lived proteins in growing fibroblasts. Papers, record 3972829. Release papers-2026-11-12-0.1.0, 12 Nov 2026. https://conductscience.org/library/papers/3972829
Paper
PubMed's record of the paper, with iCite's citation figures. No abstract is shown.
Topics11
NLM's MeSH indexing of the paper, its major topics first.
| MeSH term | Major |
|---|---|
| Adenosine Triphosphate | Major topic |
| Fibroblasts | Major topic |
| Proteins | Major topic |
| Animals | |
| Chloroquine | |
| Cricetinae | |
| Cricetulus | |
| Deoxyglucose | |
| Female | |
| Lysosomes | |
| Pregnancy |
Source PubMed
Grants2
Each grant PubMed's record writes, matched to the NIH project NIH's grant and paper links name for this paper, and each of those links the record does not write.
| Grant, as the record writes it | Agency | Country | NIH project | Stated by | Source |
|---|---|---|---|---|---|
| GM24571 | NIGMS NIH HHS | United States | R01GM024571 | PubMed and NIH | NIH RePORTER |
| NS10571 | NINDS NIH HHS | United States | R01NS010571 | PubMed and NIH | NIH RePORTER |
Cited by23
The papers in our copy of PubMed whose reference list names this one, newest first. iCite, which reads more sources, counts 103 citations.
| PMID | Title | Journal | Year | In Papers | Source |
|---|---|---|---|---|---|
| 36,768,543 | To Kill or to Be Killed: How Does the Battle between the UPS and Autophagy Maintain the Intracellular Homeostasis in Eukaryotes? | Int J Mol Sci | 2023 | https://conductscience.org/library/papers/36768543 | PubMed |
| 36,111,332 | A heterozygous p.S143P mutation in LMNA associates with proteasome dysfunction and enhanced autophagy-mediated degradation of mutant lamins A and C. | Front Cell Dev Biol | 2022 | https://conductscience.org/library/papers/36111332 | PubMed |
| 32,370,945 | Increased AMP deaminase activity decreases ATP content and slows protein degradation in cultured skeletal muscle. | Metabolism | 2020 | https://conductscience.org/library/papers/32370945 | PubMed |
| 27,022,107 | Delineation of Molecular Pathways Involved in Cardiomyopathies Caused by Troponin T Mutations. | Mol Cell Proteomics | 2016 | https://conductscience.org/library/papers/27022107 | PubMed |
| 20,634,424 | Regulation of NF-kappaB activity and inducible nitric oxide synthase by regulatory particle non-ATPase subunit 13 (Rpn13). | Proc Natl Acad Sci U S A | 2010 | https://conductscience.org/library/papers/20634424 | PubMed |
| 20,131,003 | Ubiquitin/proteasome pathway impairment in neurodegeneration: therapeutic implications. | Apoptosis | 2010 | https://conductscience.org/library/papers/20131003 | PubMed |
| 19,324,872 | T cell receptor-mediated activation of p38{alpha} by mono-phosphorylation of the activation loop results in altered substrate specificity. | J Biol Chem | 2009 | https://conductscience.org/library/papers/19324872 | PubMed |
| 17,139,257 | hRpn13/ADRM1/GP110 is a novel proteasome subunit that binds the deubiquitinating enzyme, UCH37. | EMBO J | 2006 | https://conductscience.org/library/papers/17139257 | PubMed |
| 15,601,779 | Muscle-specific RING finger 1 is a bona fide ubiquitin ligase that degrades cardiac troponin I. | Proc Natl Acad Sci U S A | 2004 | https://conductscience.org/library/papers/15601779 | PubMed |
| 12,379,695 | Inhibition of endoplasmic reticulum-associated degradation in CHO cells resistant to cholera toxin, Pseudomonas aeruginosa exotoxin A, and ricin. | Infect Immun | 2002 | https://conductscience.org/library/papers/12379695 | PubMed |
| 11,284,726 | Hierarchies of ATP-consuming processes: direct compared with indirect measurements, and comparative aspects. | Biochem J | 2001 | https://conductscience.org/library/papers/11284726 | PubMed |
| 9,716,494 | Effects of polyamine levels on the degradation of short-lived and long-lived proteins in cultured L-132 human lung cells. | Biochem J | 1998 | https://conductscience.org/library/papers/9716494 | PubMed |
| 8,878,419 | Muscle wasting in insulinopenic rats results from activation of the ATP-dependent, ubiquitin-proteasome proteolytic pathway by a mechanism including gene transcription. | J Clin Invest | 1996 | https://conductscience.org/library/papers/8878419 | PubMed |
| 8,617,877 | The acidosis of chronic renal failure activates muscle proteolysis in rats by augmenting transcription of genes encoding proteins of the ATP-dependent ubiquitin-proteasome pathway. | J Clin Invest | 1996 | https://conductscience.org/library/papers/8617877 | PubMed |
| 7,846,043 | Abnormal calcium homeostasis and mitochondrial polarization in a human encephalomyopathy. | Proc Natl Acad Sci U S A | 1995 | https://conductscience.org/library/papers/7846043 | PubMed |
| 7,492,307 | A hierarchy of ATP-consuming processes in mammalian cells. | Biochem J | 1995 | https://conductscience.org/library/papers/7492307 | PubMed |
| 3,401,210 | Distinction between major chloroquine-inhibitable and adrenergic-responsive pathways of protein degradation and their relation to tissue ATP content in the Langendorff isolated perfused rat heart. | Biochem J | 1988 | https://conductscience.org/library/papers/3401210 | PubMed |
| 3,099,758 | The activation of protein degradation in muscle by Ca2+ or muscle injury does not involve a lysosomal mechanism. | Biochem J | 1986 | https://conductscience.org/library/papers/3099758 | PubMed |
| 2,930,516 | Vanadate inhibits degradation of short-lived, but not of long-lived, proteins in L-132 human cells. | Biochem J | 1989 | https://conductscience.org/library/papers/2930516 | PubMed |
| 2,820,375 | Skeletal muscle and liver contain a soluble ATP + ubiquitin-dependent proteolytic system. | Biochem J | 1987 | https://conductscience.org/library/papers/2820375 | PubMed |
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- 2026-11-12
- Gene search
- 2026-11-11
- Pipelines
- 2026-09-18
None in this release
- Trials
- Comments and corrections
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- Drugs
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Sources 11
- ChEMBL, through Open TargetsCC BY-SA 3.0
- ClinicalTrials.govNo license stated
- HGNCCC0
- iCiteCC BY 4.0
- NCBI GenePublic domain (US government)
- NIH RePORTER's grant and paper linksPublic domain
- Open TargetsCC0 1.0
- PMC's ID filePublic domain (US government)
- PubMedNLM's terms
- PubTator 3Public domain
- UniProtCC BY 4.0
Each source's terms
- ChEMBL, through Open TargetsCC BY-SA 3.0, for the parts from ChEMBL. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
- ClinicalTrials.govnone stated
- HGNCCC0: https://www.genenames.org/about/license/
- iCiteCC BY 4.0
- NCBI GeneNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
- NIH RePORTER's grant and paper linksPublic domain (NIH RePORTER)
- Open TargetsCC0 1.0. Open Targets asks that users cite its latest paper: Buniello et al. 2025, Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery, Nucleic Acids Research 53(D1):D1467, PMID 39657122. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
- PMC's ID fileNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
- PubMedNLM's terms
- PubTator 3Public domain
- UniProtCC BY 4.0. UniProt's licence file: "All databases and documents in the UniProt FTP directory may be copied and redistributed freely, without advance permission, provided that this copyright statement is reproduced with each copy." UniProt asks that users cite its latest paper: The UniProt Consortium, UniProt: the Universal Protein Knowledgebase in 2025, Nucleic Acids Research 53:D609-D617, https://doi.org/10.1093/nar/gkae1010. Read on 9 Nov 2026 at https://www.uniprot.org/help/license
ClinicalTrials.gov's data carry an international copyright outside the United States: https://clinicaltrials.gov/about-site/terms-conditions.
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