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Protein Coding Gene : Bmx BMX non-receptor tyrosine kinase

Primary Identifier  MGI:1101778 Organism  mouse, laboratory
Chromosome  X NCBI Gene Number  12169
Mgi Type  protein coding gene
description  FUNCTION: Automated description from the Alliance of Genome Resources (Release 7.0.0)

Predicted to enable non-membrane spanning protein tyrosine kinase activity. Predicted to be involved in B cell receptor signaling pathway and adaptive immune response. Predicted to act upstream of or within apoptotic process; cell adhesion; and phosphorylation. Predicted to be located in nucleoplasm and ruffle membrane. Predicted to be active in plasma membrane. Is expressed in several structures, including cardiovascular system; central nervous system; genitourinary system; hemolymphoid system; and mammary gland. Orthologous to human BMX (BMX non-receptor tyrosine kinase).
PHENOTYPE: Mice homozygous for a null mutation are fertile and have a normal life span but are protected from arthritis in a passive transfer model. [provided by MGI curators]
  • synonyms:
  • TYRO8 protein tyrosine kinase 8,
  • MGI:109273,
  • MGD-MRK-38318,
  • Etk,
  • Bmx,
  • Etk/Bmx,
  • Tyro8,
  • BMX non-receptor tyrosine kinase

Features --> Cross References

Genome

Sequence Feature Displayer

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0 Canonical

0 CDSs

0 Exons

0 Genomic Clusters

0 Involved In Mutations

0 Strain

0 Transcripts

0 Transgenic Expressors

0 UTRs

Canonical gene --> CDSs in specific strains.

Canonical gene --> Exons in specific strains

Canonical gene --> Strain-specific IDs, biotypes, and locations

Canonical gene --> Transcripts in specific strains.

Features --> Overlapping features

Proteins

Gene --> Proteins

Function

Mouse features --> Functions (GO terms)

Homology

Genes --> Homologs

Interactions

9 Pathways

0 Targeted By

Gene --> Protein-Protein Interactions

Expression

Gene --> Expression annotations

Phenotype

Genes/Features --> Phenotypes (MP terms)

Disease

Mouse features --> Human diseases

Literature

Mouse features --> Publications

 

Other

1 Driver For