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Description:
Muskelin is a 735 amino acid nuclear and cytoplasmic protein that mediates cytoskeletal responses and cell spreading to Thrombospondin 1, an extracellular matrix glycoprotein. Forming a CTLH complex with RMND5A, Ran BP-M and TWA1, Muskelin exists as two alternatively spliced isoforms. Muskelin is implicated as an isoform-specific anchoring protein for the prostaglandin EP3 receptor, and contains one LisH domain, a CTLH domain, six Kelch repeats and an N-terminal discoidin-like domain through which it self-associates via a head-to-tail mechanism. Human and mouse Muskelin share 98% amino acid seqeuence homology and are encoded by genes located on chromosomes 7q32.3 and 6 A3.3, respectively.
Description:
APS (adapter molecule containing PH and SH2 domains), SH2-B and Lnk compose a family of adapter proteins, which contain a pleckstrin homology (PH) domain, an SH2 domain and a tyrosine phosphorylation site. Stimulation of B cell receptor (BCR) or T cell receptor (TCR) results in the phosphorylation of the immunoreceptor tyrosine-based activation motif (ITAM) of BCR, TCR and several substrates. APS, SH2-B and Lnk may bind to the ITAM domain of BCR and TCR. Lnk is tyrosine phosphorylated in response to TCR stimulation and APS has been shown to be tyrosine phosphorylated in response to BCR stimulation.
Description:
Pinch is a focal adhesion protein that is a component of the ILK-PINCH complex. This complex is a major part of the growth factor and integrin signaling pathway. Pinch is involved in cell differentiation, proliferation and survival by acting as an effector of integrin and growth factor signaling. It is a cytoplasmic protein expressed in most tissues and consists of five LIM domains, a nuclear localization signal and a nuclear export signal. The PINCH-1/ILK complex is regulated by another member of the Pinch family, PINCH-2, which also forms a complex with ILK.
Description:
Chromosome 9 consists of about 145 million bases and 4% of the human genome and encodes nearly 900 genes. Considered to play a role in gender determination, deletion of the distal portion of 9p can lead to development of male to female sex reversal, the phenotype of a female with a male X,Y genotype. Hereditary hemorrhagic telangiectasia, which is characterized by harmful vascular defects, is associated with the chromosome 9 gene encoding endoglin protein, ENG. Familial dysautonomia is also associated with chromosome 9 though through the gene IKBKAP. Notably, chromosome 9 encompasses the largest interferon family gene cluster. Chromosome 9 is partnered with chromosome 22 in the translocation leading to the aberrant production of BCR-ABL fusion protein often found in leukemias. The C9orf64 gene product has been provisionally designated C9orf64 pending further characterization.
Description:
Chromosome 9 consists of about 145 million bases and 4% of the human genome and encodes nearly 900 genes. Considered to play a role in gender determination, deletion of the distal portion of 9p can lead to development of male to female sex reversal, the phenotype of a female with a male X,Y genotype. Hereditary hemorrhagic telangiectasia, which is characterized by harmful vascular defects, is associated with the chromosome 9 gene encoding endoglin protein, ENG. Familial dysautonomia is also associated with chromosome 9 though through the gene IKBKAP. Notably, chromosome 9 encompasses the largest interferon family gene cluster. Chromosome 9 is partnered with chromosome 22 in the translocation leading to the aberrant production of BCR-ABL fusion protein often found in leukemias. The C9orf57 gene product has been provisionally designated C9orf57 pending further characterization.
Description:
Chromosome 9 consists of about 145 million bases and 4% of the human genome and encodes nearly 900 genes. Considered to play a role in gender determination, deletion of the distal portion of 9p can lead to development of male to female sex reversal, the phenotype of a female with a male X,Y genotype. Hereditary hemorrhagic telangiectasia, which is characterized by harmful vascular defects, is associated with the chromosome 9 gene encoding endoglin protein, ENG. Familial dysautonomia is also associated with chromosome 9 though through the gene IKBKAP. Notably, chromosome 9 encompasses the largest interferon family gene cluster. Chromosome 9 is partnered with chromosome 22 in the translocation leading to the aberrant production of BCR-ABL fusion protein often found in leukemias. The C9orf66 gene product has been provisionally designated C9orf66 pending further characterization.
Description:
Chromosome 9 consists of about 145 million bases and 4% of the human genome and encodes nearly 900 genes. Considered to play a role in gender determination, deletion of the distal portion of 9p can lead to development of male to female sex reversal, the phenotype of a female with a male X,Y genotype. Hereditary hemorrhagic telangiectasia, which is characterized by harmful vascular defects, is associated with the chromosome 9 gene encoding endoglin protein, ENG. Familial dysautonomia is also associated with chromosome 9 though through the gene IKBKAP. Notably, chromosome 9 encompasses the largest interferon family gene cluster. Chromosome 9 is partnered with chromosome 22 in the translocation leading to the aberrant production of BCR-ABL fusion protein often found in leukemias. The C9orf84 gene product has been provisionally designated C9orf84 pending further characterization. There are two isoforms of C9orf84 that are produced as a result of alternative splicing events.
Description:
This gene encodes a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily. Members of this family share a common protein fold and have diverse functions, such as cell adhesion, cell-cell signalling, glycoprotein turnover, and roles in inflammation and immune response. The encoded protein may play a role in regulating dendritic cell function. Alternative splice variants have been described but their biological nature has not been determined. This gene is closely linked to other CTL/CTLD superfamily members on chromosome 12p13 in the natural killer gene complex region. [provided by RefSeq]
Description:
The transcription factor NFkB is retained in the cytoplasm in an inactive form by the inhibitory protein IkB. Activation of NFkB requires that IkB be phosphorylated on specific serine residues, which results in the targeted degradation of IkB (1). IkB kinase alpha (IKK alpha), previously designated CHUK (2), interacts with IkB-alpha and specifically phosphorylates IkB-alpha on the sites that trigger its degradation, serines 32 and 36 (3). IKKalpha appears to be critical for NFkB activation in response to proinflammatory cytokines (4). Phosphorylation of the IkB by IKK alpha is stimulated by the NFkB inducing kinase (NIK), which itself is a central regulator for NFkB activation in response to TNF and IL-1 (5). The functional IKK complex contains three subunits, IKK alpha, IKK beta and IKK gamma (also designated NEMO), and each appears to make essential contributions to IkB phosphorylation (6). IKAP (IKK-complex-associated protein) is a protein that acts as a scaffold, interacting with NIK, IKK alpha and IKK beta and assembling them into an active kinase complex (7,8)
Description:
Kinase-defective receptor for members of the ephrin-B family. Binds to ephrin-B1 and ephrin-B2. Modulates cell adhesion and migration by exerting both positive and negative effects upon stimulation with ephrin-B2. Inhibits JNK activation, T-cell receptor-induced IL-2 secretion and CD25 expression upon stimulation with ephrin-B2.
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