Shb src homology 2 domain-containing transforming protein B [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Shbprovided by MGI
Official Full Name: src homology 2 domain-containing transforming protein Bprovided by MGI
Primary source: MGI:MGI:98294
See related: Ensembl:ENSMUSG00000044813 AllianceGenome:MGI:98294
Gene type: protein coding
RefSeq status: VALIDATED
Organism: Mus musculus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus
Summary: Enables signaling receptor complex adaptor activity. Acts upstream of or within several processes, including hematopoietic stem cell proliferation; negative regulation of oocyte maturation; and positive regulation of immune response. Predicted to be located in cytoplasmic ribonucleoprotein granule; cytosol; and nucleoplasm. Is expressed in brain; molar; and sensory organ. Orthologous to human SHB (SH2 domain containing adaptor protein B). [provided by Alliance of Genome Resources, Nov 2024]
Expression: Broad expression in adrenal adult (RPKM 54.6), duodenum adult (RPKM 22.8) and 25 other tissues See more
Orthologs: human all
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Genomic context

Location:: 4 B1; 4 24.0 cM

Exon count:: 6

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	4	NC_000070.7 (45423278..45530804, complement)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	4	NC_000070.6 (45423276..45530828, complement)

Chromosome 4 - NC_000070.7 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

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Expression

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See details

Project title: Mouse ENCODE transcriptome data
Description: RNA profiling data sets generated by the Mouse ENCODE project.
BioProject: PRJNA66167
Publication: PMID 25409824
Analysis date: n/a

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

Absence of the Shb gene in mixed-lineage leukemia MLL-AF9 cells increases latency in mice despite higher proliferation rates in vitro.
Title: Absence of the Shb gene in mixed-lineage leukemia MLL-AF9 cells increases latency in mice despite higher proliferation rates in vitro.
Pericyte dysfunction due to Shb gene deficiency increases B16F10 melanoma lung metastasis.
Title: Pericyte dysfunction due to Shb gene deficiency increases B16F10 melanoma lung metastasis.
The absence of the src homology 2 domain-containing transforming protein B (Shb) gene exacerbates the disease in myeloid leukemia, whereas it alters the disease characteristics without affecting latency in B- and T-cell leukemia.
Title: Disparate effects of Shb gene deficiency on disease characteristics in murine models of myeloid, B-cell, and T-cell leukemia.
The observed aberrations in myeloid cell properties in Shb-deficient mice are likely consequences of an abnormal vascular compartment and are not responsible for reduced muscle blood flow
Title: Shb deficiency in endothelium but not in leucocytes is responsible for impaired vascular performance during hindlimb ischaemia.
a unique combinatorial response of increased vascular permeability and reduced recruitment of cytotoxic CD8+ cells occurs as a consequence of Shb deficiency in B16F10 melanomas.
Title: Vascular dysfunction and increased metastasis of B16F10 melanomas in Shb deficient mice as compared with their wild type counterparts.
Data indicate that Src homology-2 domain containing protein B (SHB) deficiency causes a chronic increase in beta-cell focal adhesion kinase (FAK) activity that perturbs the normal insulin secretory characteristics of beta-cells.
Title: Absence of Shb impairs insulin secretion by elevated FAK activity in pancreatic islets.
Data suggest that absence of Src homology-2 protein Shb accelerates disease progression by exerting dual roles in BCR-ABL-induced leukemia: increased cell expansion due to elevated focal adhesion kinase (FAK) activity and neutrophilia in peripheral blood.
Title: The Src homology-2 protein Shb modulates focal adhesion kinase signaling in a BCR-ABL myeloproliferative disorder causing accelerated progression of disease.
loss of Shb alters TCR signalling ability, thereby favouring the development of Th2-driven inflammation and exacerbating symptoms of allergy
Title: Absence of the adaptor protein Shb potentiates the T helper type 2 response in a mouse model of atopic dermatitis.
Shb knockout mouse exhibited structural and functional (angiogenesis and vascular permeability) vascular abnormalities that have implications for understanding the function of VEGF-A under physiological conditions
Title: Vascular adaptation to a dysfunctional endothelium as a consequence of Shb deficiency.
Data show reduced VEGF-A expression in Shb-deficient tumors.Interference with Shb signaling may provide novel means for future cancer therapy.
Title: Heterogeneity among RIP-Tag2 insulinomas allows vascular endothelial growth factor-A independent tumor expansion as revealed by studies in Shb mutant mice: implications for tumor angiogenesis.

Submit: New GeneRIF Correction See all GeneRIFs (21)

Variation

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Alleles

Alleles of this type are documented at Mouse Genome Informatics (MGI)

Endonuclease-mediated (1)
Targeted (3) 1 citation

Interactions

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Products	Interactant	Other Gene	Complex	Source	Pubs	Description

General gene information

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Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables phosphotyrosine residue binding	IBA Inferred from Biological aspect of Ancestor more info
enables phosphotyrosine residue binding	IEA Inferred from Electronic Annotation more info
enables phosphotyrosine residue binding	ISO Inferred from Sequence Orthology more info
enables signaling receptor complex adaptor activity	IDA Inferred from Direct Assay more info	PubMed

Process	Evidence Code	Pubs
acts_upstream_of_or_within B cell proliferation	IDA Inferred from Direct Assay more info	PubMed
acts_upstream_of_or_within T cell receptor signaling pathway	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in angiogenesis	IEA Inferred from Electronic Annotation more info
involved_in apoptotic process	IEA Inferred from Electronic Annotation more info
acts_upstream_of_or_within blood vessel development	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within blood vessel morphogenesis	IGI Inferred from Genetic Interaction more info	PubMed
acts_upstream_of_or_within blood vessel morphogenesis	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within hematopoietic stem cell proliferation	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within hemopoiesis	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within negative regulation of oocyte maturation	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within negative regulation of protein kinase activity	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within positive regulation of T-helper cell differentiation	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within positive regulation of mitotic cell cycle	IMP Inferred from Mutant Phenotype more info	PubMed

Component	Evidence Code	Pubs
located_in cytoplasmic ribonucleoprotein granule	IEA Inferred from Electronic Annotation more info
located_in cytoplasmic ribonucleoprotein granule	ISO Inferred from Sequence Orthology more info
located_in cytosol	IEA Inferred from Electronic Annotation more info
located_in cytosol	ISO Inferred from Sequence Orthology more info
located_in nucleoplasm	IEA Inferred from Electronic Annotation more info
located_in nucleoplasm	ISO Inferred from Sequence Orthology more info
located_in plasma membrane	IEA Inferred from Electronic Annotation more info

General protein information

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Preferred Names: SH2 domain-containing adapter protein B

NCBI Reference Sequences (RefSeq)

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RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above.