Approaching the multifaceted nature of energy metabolism: inactivation of the cytosolic creatine kinases via homologous recombination in mouse embryonic stem cells.

doi:10.1007/BF01267959

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

Back to search

Article

Approaching the multifaceted nature of energy metabolism: inactivation of the cytosolic creatine kinases via homologous recombination in mouse embryonic stem cells.

Molecular and cellular biochemistry - 1 Jan 2000

van Deursen J, Wieringa B

Abstract excerpt

To study the physiological role of the creatine kinase/phosphocreatine (CK/PCr) system in cells and tissues with a high and fluctuating energy demand we have concentrated on the site-directed inactivation of the B- and M-CK genes encoding the cytosolic CK protein subunits. In our approach we used homologous recombination in mouse embryonic stem (ES) cells from strain 129/Sv. Using targeting constructs based on...

Topics

Animals
Chimera
Creatine Kinase
Cytosol
Embryo, Mammalian
Energy Metabolism
Female
Genetic Vectors
Isoenzymes
Male
Mice
Mice, Inbred C57BL

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Mice, Inbred CBA

Mice, Knockout

Muscles

Phenotype

Pregnancy

Recombination, Genetic

Source

Open in PubMed

Identifiers

PMID: 7808458
DOI: 10.1007/BF01267959

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-7808458-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

discussions

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Approaching the multifaceted nature of energy metabolism: inactivation of the cytosolic creatine kinases via homologous recombination in mouse embryonic stem cells.PMID 7808458Read ↗

Creatine kinase (CK) in skeletal muscle energy metabolism: a study of mouse mutants with graded reduction in muscle CK expression.Semantic proximity Read ↗

Modulation of gene activity by consecutive gene targeting of one creatine kinase M allele in mouse embryonic stem cells.Semantic proximity Read ↗

Bioenergetics. Dissecting the role of creatine kinase.Semantic proximity Read ↗

Cytoarchitectural and metabolic adaptations in muscles with mitochondrial and cytosolic creatine kinase deficiencies.Semantic proximity Read ↗

Creatine kinase knockout mice--what is the phenotype: heart.Semantic proximity Read ↗

Mouse ubiquitous mitochondrial creatine kinase: gene organization and consequences from inactivation in mouse embryonic stem cells.Semantic proximity Read ↗

Creatine kinase knockout mice--what is the phenotype: skeletal muscle.Semantic proximity Read ↗

Cardiac phenotype of mitochondrial creatine kinase knockout mice is modified on a pure C57BL/6 genetic background.Semantic proximity Read ↗

Altered Ca2+ responses in muscles with combined mitochondrial and cytosolic creatine kinase deficiencies.Semantic proximity Read ↗

Creatine metabolism and the consequences of creatine depletion in muscle.Semantic proximity Read ↗

Myofibrillar or mitochondrial creatine kinase deficiency alone does not impair mouse diaphragm isotonic function.Semantic proximity Read ↗

Combined myofibrillar and mitochondrial creatine kinase deficiency impairs mouse diaphragm isotonic function.Semantic proximity Read ↗

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