MGI:1922721 GO curators for mouse genes have assigned the following annotations to the gene product of 1700009N14Rik. (This text reflects annotations as of Thursday, May 31, 2012.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of February 7, 2008. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text for additional MGI annotations
References
  1. Huang J et al. (2007) Very-KIND, a KIND domain containing RasGEF, controls dendrite growth by linking Ras small GTPases and MAP2. J Cell Biol, 179:539-52. (PubMed:17984326)
MGI:2443767 GO curators for mouse genes have assigned the following annotations to the gene product of Aaas. (This text reflects annotations as of Thursday, May 31, 2012.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of July 11, 2007. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.
Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] The protein encoded by this gene is a member of the WD-repeat family of regulatory proteins and may be involved in normal development of the peripheral and central nervous system. The encoded protein is part of the nuclear pore complex and is anchored there by NDC1. Defects in this gene are a cause of achalasia-addisonianism-alacrima syndrome (AAAS), also called triple-A syndrome or Allgrove syndrome. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Mar 2010]
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text for additional MGI annotations
References
  1. Huebner A et al. (2006) Mice lacking the nuclear pore complex protein ALADIN show female infertility but fail to develop a phenotype resembling human triple A syndrome. Mol Cell Biol, 26:1879-87. (PubMed:16479006)
MGI:1926144 GO curators for mouse genes have assigned the following annotations to the gene product of Aacs. (This text reflects annotations as of Thursday, May 31, 2012.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of February 2, 2010. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text based on GO annotations supported by structural data
Summary text for additional MGI annotations
MGI:1929608 GO curators for mouse genes have assigned the following annotations to the gene product of Aatf. (This text reflects annotations as of Thursday, May 31, 2012.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of August 29, 2008. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.
Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] The protein encoded by this gene was identified on the basis of its interaction with MAP3K12/DLK, a protein kinase known to be involved in the induction of cell apoptosis. This gene product contains a leucine zipper, which is a characteristic motif of transcription factors, and was shown to exhibit strong transactivation activity when fused to Gal4 DNA binding domain. Overexpression of this gene interfered with MAP3K12 induced apoptosis. [provided by RefSeq, Jul 2008]
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text based on GO annotations supported by experimental evidence in other organisms
References
  1. Guo Q et al. (2004) AATF inhibits aberrant production of amyloid beta peptide 1-42 by interacting directly with Par-4. J Biol Chem, 279:4596-603. (PubMed:14627703)
  2. Thomas T et al. (2000) The murine gene, traube, is essential for the growth of preimplantation embryos Dev Biol, 227:324-42. (PubMed:11071758)
MGI:1197518 GO curators for mouse genes have assigned the following annotations to the gene product of Aatk. (This text reflects annotations as of Thursday, May 31, 2012.)
Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] The protein encoded by this gene contains a tyrosine kinase domain at the N-terminus and a proline-rich domain at the C-terminus. This gene is induced during apoptosis, and expression of this gene may be a necessary pre-requisite for the induction of growth arrest and/or apoptosis of myeloid precursor cells. This gene has been shown to produce neuronal differentiation in a neuroblastoma cell line. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jun 2011]
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text based on GO annotations supported by structural data
Summary text for additional MGI annotations
References
  1. Gaozza E et al. (1997) AATYK: a novel tyrosine kinase induced during growth arrest and apoptosis of myeloid cells. Oncogene, 15:3127-35. (PubMed:9444961)
  2. Tomomura M et al. (2007) Structural and functional analysis of the apoptosis-associated tyrosine kinase (AATYK) family. Neuroscience, 148:510-21. (PubMed:17651901)
MGI:88025 GO curators for mouse genes have assigned the following annotations to the gene product of Ank2. (This text reflects annotations as of Thursday, May 31, 2012.)
Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a member of the ankyrin family of proteins that link the integral membrane proteins to the underlying spectrin-actin cytoskeleton. Ankyrins play key roles in activities such as cell motility, activation, proliferation, contact and the maintenance of specialized membrane domains. Most ankyrins are typically composed of three structural domains: an amino-terminal domain containing multiple ankyrin repeats; a central region with a highly conserved spectrin binding domain; and a carboxy-terminal regulatory domain which is the least conserved and subject to variation. The protein encoded by this gene is required for targeting and stability of Na/Ca exchanger 1 in cardiomyocytes. Mutations in this gene cause long QT syndrome 4 and cardiac arrhythmia syndrome. Multiple transcript variants encoding different isoforms have been described. [provided by RefSeq, Dec 2011]
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text based on GO annotations supported by structural data
Summary text for additional MGI annotations
References
  1. Kizhatil K et al. (2009) Ankyrin-B is required for coordinated expression of beta-2-spectrin, the Na/K-ATPase and the Na/Ca exchanger in the inner segment of rod photoreceptors. Exp Eye Res, 88:57-64. (PubMed:19007774)
  2. Mohler PJ et al. (2004) Ankyrin-B targets beta2-spectrin to an intracellular compartment in neonatal cardiomyocytes. J Biol Chem, 279:40185-93. (PubMed:15262991)
MGI:88180 GO curators for mouse genes have assigned the following annotations to the gene product of Bmp4. (This text reflects annotations as of Thursday, May 31, 2012.)
Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] The protein encoded by this gene is a member of the bone morphogenetic protein family which is part of the transforming growth factor-beta superfamily. The superfamily includes large families of growth and differentiation factors. Bone morphogenetic proteins were originally identified by an ability of demineralized bone extract to induce endochondral osteogenesis in vivo in an extraskeletal site. This particular family member plays an important role in the onset of endochondral bone formation in humans, and a reduction in expression has been associated with a variety of bone diseases, including the heritable disorder Fibrodysplasia Ossificans Progressiva. Alternative splicing in the 5' untranslated region of this gene has been described and three variants are described, all encoding an identical protein. [provided by RefSeq, Jul 2008]
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text based on GO annotations supported by structural data
Summary text for additional MGI annotations
References
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  32. Lenox LE et al. (2005) BMP4 and Madh5 regulate the erythroid response to acute anemia. Blood, 105:2741-8. (PubMed:15591122)
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MGI:2448549 GO curators for mouse genes have assigned the following annotations to the gene product of Cdk10. (This text reflects annotations as of Thursday, May 31, 2012.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of February 2, 2010. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.
Summary from NCBI RefSeq

The protein encoded by this gene belongs to the CDK (cyclin-dependent kinase) subfamily of the Ser/Thr protein kinase family. The CDK subfamily members are highly similar to the gene products of S. cerevisiae cdc28, and S. pombe cdc2, and are known to be essential for cell cycle progression. The human ortholog has been shown to play a role in cellular proliferation. Multiple transcript variants encoding different isoforms have been found for this gene. A related pseudogene exists on chromosome 1. [provided by RefSeq, Jan 2010]
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text based on GO annotations supported by structural data
Summary text for additional MGI annotations
MGI:88276 GO curators for mouse genes have assigned the following annotations to the gene product of Ctnnb1. (This text reflects annotations as of Thursday, May 31, 2012.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of March 26, 2010. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.
Summary from NCBI RefSeq

This gene encodes not only an important cytoplasmic component of the classical cadherin adhesion complex that forms the adherens junction in epithelia and mediates cell-cell adhesion in many other tissues but also a key signaling molecule in the canonical Wnt signaling pathway that controls cell growth and differentiation during both normal development and tumorigenesis. The gene product contains a central armadillo-repeat containing domain through which it binds the cytoplasmic tail of classical cadherins; meanwhile, it also binds alpha-catenin, which further links the cadherin complex to the actin cytoskeleton either directly or indirectly. Beta-catenin is therefore necessary for the adhesive function of classical cadherins. Another key function of this protein is to mediate the canonical Wnt signaling pathway and regulate gene transcription. Without Wnt signal, cytoplasmic beta-catenin that is not associated with the cadherin complex is quickly phosphorylated at the N-terminal Ser/Thr residues by the so called degradation complex containing axin, adenomatous polyposis coli (APC), casein kinase I, and GSK3B, then ubiquitylated by beta-TrCP, and degraded by the proteasome. However, in the presence of Wnt signal, the degradation complex is disrupted and the stabilized cytoplasmic beta-catenin translocates into the nucleus, where it binds various transcription factors and, together with these factors, regulates the transcription of many downstream genes. Mutations of this gene have been linked with various types of tumors. Alternatively spliced variants have been found for this gene. [provided by RefSeq, Sep 2009]
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text based on GO annotations supported by structural data
Summary text for additional MGI annotations
References
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MGI:98297 GO curators for mouse genes have assigned the following annotations to the gene product of Shh. (This text reflects annotations as of Thursday, May 31, 2012.)
Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a protein that is instrumental in patterning the early embryo. It has been implicated as the key inductive signal in patterning of the ventral neural tube, the anterior-posterior limb axis, and the ventral somites. Of three human proteins showing sequence and functional similarity to the sonic hedgehog protein of Drosophila, this protein is the most similar. The protein is made as a precursor that is autocatalytically cleaved; the N-terminal portion is soluble and contains the signalling activity while the C-terminal portion is involved in precursor processing. More importantly, the C-terminal product covalently attaches a cholesterol moiety to the N-terminal product, restricting the N-terminal product to the cell surface and preventing it from freely diffusing throughout the developing embryo. Defects in this protein or in its signalling pathway are a cause of holoprosencephaly (HPE), a disorder in which the developing forebrain fails to correctly separate into right and left hemispheres. HPE is manifested by facial deformities. It is also thought that mutations in this gene or in its signalling pathway may be responsible for VACTERL syndrome, which is characterized by vertebral defects, anal atresia, tracheoesophageal fistula with esophageal atresia, radial and renal dysplasia, cardiac anomalies, and limb abnormalities. Additionally, mutations in a long range enhancer located approximately 1 megabase upstream of this gene disrupt limb patterning and can result in preaxial polydactyly. [provided by RefSeq, Jul 2008]
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text based on GO annotations supported by structural data
Summary text for additional MGI annotations
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MGI:2685277 GO curators for mouse genes have assigned the following annotations to the gene product of Zyg11b. (This text reflects annotations as of Thursday, May 31, 2012.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of April 30, 2012. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.
Summary text for additional MGI annotations
MGI:103072 GO curators for mouse genes have assigned the following annotations to the gene product of Zyx. (This text reflects annotations as of Thursday, May 31, 2012.)
Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] Focal adhesions are actin-rich structures that enable cells to adhere to the extracellular matrix and at which protein complexes involved in signal transduction assemble. Zyxin is a zinc-binding phosphoprotein that concentrates at focal adhesions and along the actin cytoskeleton. Zyxin has an N-terminal proline-rich domain and three LIM domains in its C-terminal half. The proline-rich domain may interact with SH3 domains of proteins involved in signal transduction pathways while the LIM domains are likely involved in protein-protein binding. Zyxin may function as a messenger in the signal transduction pathway that mediates adhesion-stimulated changes in gene expression and may modulate the cytoskeletal organization of actin bundles. Alternative splicing results in multiple transcript variants that encode the same isoform. [provided by RefSeq, Jul 2008]
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text based on GO annotations supported by structural data
Summary text for additional MGI annotations
References
  1. Keicher C et al. (2004) Phosphorylation of mouse LASP-1 on threonine 156 by cAMP- and cGMP-dependent protein kinase. Biochem Biophys Res Commun, 324:308-16. (PubMed:15465019)
MGI:2444286 GO curators for mouse genes have assigned the following annotations to the gene product of Zzef1. (This text reflects annotations as of Thursday, May 31, 2012.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of February 2, 2010. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.
Summary text based on GO annotations supported by structural data
Summary text for additional MGI annotations
MGI:1920453 GO curators for mouse genes have assigned the following annotations to the gene product of Zzz3. (This text reflects annotations as of Thursday, May 31, 2012.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of February 9, 2010. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.
Summary text based on GO annotations supported by structural data
Summary text for additional MGI annotations