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SH3-domain GRB2-like 1

fusion partner of MLL
This gene encodes a member of the endophilin family of Src homology 3 domain-containing proteins. The encoded protein is involved in endocytosis and may also play a role in the cell cycle. Overexpression of this gene may play a role in leukemogenesis, and the encoded protein has been implicated in acute myeloid leukemia as a fusion partner of the myeloid-lymphoid leukemia protein. Pseudogenes of this gene are located on the long arm of chromosomes 11 and 17. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene. [provided by RefSeq, Jan 2011] (from NCBI)
Top mentioned proteins: MLL, HAD, SET, U19, p13
Papers on fusion partner of MLL
Complex MLL rearrangement in non-infiltrated bone marrow in an infant with stage II precursor B-lymphoblastic lymphoma.
Rossig et al., Münster, Germany. In Eur J Haematol, 2014
METHODS: Cytogenetic analysis was performed by fluorescence in situ hybridization (FISH), and the genomic fusion partner of MLL was identified by long-distance inverse (LDI-)PCR and confirmed by direct PCR.
Epidemiological survey of idiopathic scoliosis and sequence alignment analysis of multiple candidate genes.
Hou et al., Chongqing, China. In Int Orthop, 2012
Idiopathic scoliosis is a multifactorial genetic disease and SH3GL1 may be one of the pathogenic genes for this disease.
Proteomic analysis identifies dysfunction in cellular transport, energy, and protein metabolism in different brain regions of atypical frontotemporal lobar degeneration.
Bahn et al., Cambridge, United Kingdom. In J Proteome Res, 2012
A protein encoded by this locus was found to be differentially expressed in postmortem brains from patients with atypical frontotemporal lobar degeneration.
[Comparative analysis of sequence alignment of SH3GL1 gene as a disease candidate gene of adolescent idiopathic scoliosis].
Bai et al., Chongqing, China. In Zhonghua Wai Ke Za Zhi, 2010
SH3GL1 is possibly one of the disease associated genes of adolescent idiopathic scoliosis.
A variant-type MLL/SEPT9 fusion transcript in adult de novo acute monocytic leukemia (M5b) with t(11;17)(q23;q25).
Miura et al., Tokyo, Japan. In Int J Hematol, 2008
SEPT9 is a very rare but recurrent fusion partner of MLL, and has recently been implicated in the oncogenesis of various malignancies.
Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA.
Taniwaki et al., Kyoto, Japan. In Oncogene, 2008
The LAF4 gene is a member of the AF4/FMR2 family and was previously identified as a fusion partner of MLL in B-precursor ALL with t(2;11)(q11;q23), although AML1-LAF4 was in T-ALL.
Identification of a novel fusion gene MLL-MAML2 in secondary acute myelogenous leukemia and myelodysplastic syndrome with inv(11)(q21q23).
Nagasawa et al., Tsukuba, Japan. In Genes Chromosomes Cancer, 2007
We have identified a novel fusion partner of MLL, namely the mastermind like 2 (MAML2 gene), in secondary acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) with inv(11)(q21q23).
FB1, an E2A fusion partner in childhood leukemia, interacts with U19/EAF2 and inhibits its transcriptional activity.
Wang et al., Chicago, United States. In Cancer Lett, 2007
U19/EAF2 has also been identified as ELL-associated factor 2 (EAF2) based on its binding to ELL, a fusion partner of MLL in acute myeloid leukemia.
Apoptosis induction and growth suppression by U19/Eaf2 is mediated through its ELL-binding domain.
Wang et al., Chicago, United States. In Prostate, 2007
U19/Eaf2 interacts with ELL, a fusion partner of MLL in the (11;19) (q23;p13.1)
SEPT2 is a new fusion partner of MLL in acute myeloid leukemia with t(2;11)(q37;q23).
Teixeira et al., Porto, Portugal. In Oncogene, 2006
Fluorescence in situ hybridization demonstrated a rearrangement of the MLL gene and molecular genetic analyses identified a septin family gene, SEPT2, located on chromosome 2q37, as the fusion partner of MLL.
Activation of EGF receptor endocytosis and ERK1/2 signaling by BPGAP1 requires direct interaction with EEN/endophilin II and a functional RhoGAP domain.
Low et al., Singapore, Singapore. In J Cell Sci, 2005
findings reveal a concomitant activation of endocytosis and ERK signaling by BPGAP1 via the coupling of its proline-rich region, which targets EEN and its functional GAP domain
Subcellular localization of EEN/endophilin A2, a fusion partner gene in leukaemia.
Chan et al., Hong Kong, Hong Kong. In Biochem J, 2004
Our results suggest that distinct subcellular localization of the endophilin A family members probably underpins their diverse cellular functions and indicates a role for EEN/EA2 in the cell cycle.
Molecular genetics of the Alhambra (Drosophila AF10) complex locus of Drosophila.
Dura et al., Montpellier, France. In Mol Genet Genomics, 2004
AF10 has been identified as a fusion partner of MLL, a human homologue of the fly gene trithorax, in infant leukemias.
The small oligomerization domain of gephyrin converts MLL to an oncogene.
Greaves et al., London, United Kingdom. In Blood, 2004
Here we show that gephyrin (GPHN), a neuronal receptor assembly protein and rare fusion partner of MLL in leukemia, has the capacity as an MLL-GPHN chimera to transform hematopoietic progenitors, despite lack of transcriptional activity.
Altered expression of the septin gene, SEPT9, in ovarian neoplasia.
Russell et al., Belfast, United Kingdom. In J Pathol, 2003
a region commonly deleted in sporadic ovarian and breast tumours, and has also been identified as a fusion partner of MLL in acute myeloid leukaemias.
The LIM domain protein Lmo2 binds to AF6, a translocation partner of the MLL oncogene.
Leutz et al., Berlin, Germany. In Febs Lett, 2002
AF6 is a recurrent fusion partner of MLL, the human homolog of Drosophila trithorax chromatin remodeling protein that is involved in childhood leukemia and mixed lineage leukemia.
Genomic organization, complex splicing pattern and expression of a human septin gene on chromosome 17q25.3.
Russell et al., Belfast, United Kingdom. In Oncogene, 2001
The Ov/Br septin gene, which is also a fusion partner of MLL in acute myeloid leukaemia, is a member of a family of novel GTP binding proteins that have been implicated in cytokinesis and exocytosis.
The synovial sarcoma associated protein SYT interacts with the acute leukemia associated protein AF10.
Geurts van Kessel et al., Nijmegen, Netherlands. In Oncogene, 2001
Of the positive clones isolated, two were found to correspond to the acute leukemia t(10;11) associated AF10 gene, a fusion partner of MLL.
Genomic organization, tissue expression, and cellular localization of AF3p21, a fusion partner of MLL in therapy-related leukemia.
Sano et al., Kōbe, Japan. In Genes Chromosomes Cancer, 2001
We previously identified the AF3p21 gene, a novel fusion partner of the MLL gene, in a patient who had developed therapy-related leukemia with t(3;11)(p21;q23).
The interaction between EEN and Abi-1, two MLL fusion partners, and synaptojanin and dynamin: implications for leukaemogenesis.
Chan et al., Hong Kong, Hong Kong. In Leukemia, 2000
Using GST pull down and the yeast two hybrid system, we show that two different MLL fusion partners with SH3 domains, EEN and Abi-1, interact with dynamin and synaptojanin, both of which are involved in endocytosis.
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