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Keratin 33A

hHa3-I, K33A, HA-31
The protein encoded by this gene is a member of the keratin gene family. It is one of the type I hair keratin genes which are clustered in a region of chromosome 17q12-q21 and have the same direction of transcription. As a type I hair keratin, it is an acidic protein which heterodimerizes with type II keratins to form hair and nails. There are two isoforms of this protein, encoded by two separate genes, KRTHA3A and KRTHA3B. [provided by RefSeq, Jul 2008] (from NCBI)
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Top mentioned proteins: HAIR, cytokeratin, HA-8, Lysozyme, POLYMERASE
Papers on hHa3-I
The Red clover necrotic mosaic virus capsid protein N-terminal lysine-rich motif is a determinant of symptomatology and virion accumulation.
Lommel et al., Seoul, South Korea. In Mol Plant Pathol, 2012
Three other ASMs (K25A, K33A and K38A) displayed milder symptoms and significant reductions in virion accumulation when compared with wild-type RCNMV, but retained the ability to spread systemically.
Crystal structures of K33 mutant hen lysozymes with enhanced activities.
Ueda et al., Fukuoka, Japan. In J Biochem, 2008
In order to examine the effects of mutation of K33N on enzyme activity, we prepared K33N and K33A mutant lysozymes from yeast.
Relationship between the stability of hen egg-white lysozymes mutated at sites designed to interact with alpha-helix dipoles and their secretion amounts in yeast.
Kato et al., Yamaguchi, Japan. In Biosci Biotechnol Biochem, 2007
The positively charged lysine at the C-terminals of three long alpha-helices (5-15, 25-35, and 88-99) was replaced with alanine (K13A, K33A, K97A) or aspartic acid (K13D, K33D, K97D) in hen lysozyme by genetic engineering.
Basic residues in the Mason-Pfizer monkey virus gag matrix domain regulate intracellular trafficking and capsid-membrane interactions.
Hunter et al., Atlanta, United States. In J Virol, 2007
Electron microscopy of mutant Gag-expressing cells revealed four distinct phenotypes: K16A and K20A immature capsids accumulated on and budded into intracellular vesicles; R10A, K27A, and R22A capsid transport was arrested at the cellular cortical actin network, while K25A immature capsids were dispersed throughout the cytoplasm and appeared to be defective at an earlier stage of intracellular transport; and the remaining mutant (K33A and K39A) capsids accumulated at the inner surface of the plasma membrane.
The human type I keratin gene family: characterization of new hair follicle specific members and evaluation of the chromosome 17q21.2 gene domain.
Schweizer et al., Heidelberg, Germany. In Differentiation, 2004
This study reports the isolation of cDNA sequences for these keratin genes, termed K25irs1-K25irs4, Ka35, and Ka36, as well as cDNA sequences for the previously reported hair keratins hHa3-I, hHa7, and hHa8.
The effect of silica-containing calcium-phosphate particles on human osteoblasts in vitro.
Frondoza et al., Baltimore, United States. In J Biomed Mater Res A, 2004
Three newly synthesized silica-containing bioactive glass formulations, HA-31 (25%), HA-11 (50%), and HA-13 (75%), were tested as biocompatible substrates for the continued proliferation and phenotype expression of human bone cells in vitro.
Characterization of a cluster of human high/ultrahigh sulfur keratin-associated protein genes embedded in the type I keratin gene domain on chromosome 17q12-21.
Schweizer et al., Heidelberg, Germany. In J Biol Chem, 2001
The center of the cluster, starting 35 kb downstream of the hHa3-I hair keratin gene, contained 37 genes for high/ultrahigh sulfur hair keratin-associated proteins (KAPs), which could be divided into a total of 7 KAP multigene families based on amino acid homology comparisons with previously identified sheep, mouse, and rabbit KAPs.
A single arginyl residue in plastocyanin and in cytochrome c(6) from the cyanobacterium Anabaena sp. PCC 7119 is required for efficient reduction of photosystem I.
De la Rosa et al., Sevilla, Spain. In J Biol Chem, 2001
Other mutations concern specific residues of plastocyanin either at its positively charged east face (D49K, H57A, H57E, K58A, K58E, Y83A, and Y83F) or at its north hydrophobic pole (L12A, K33A, and K33E).
Anti-very late antigen-1 monoclonal antibody modulates the development of secondary lesion and T-cell response in experimental arthritis.
Cirino et al., Napoli, Italy. In Lab Invest, 2000
In vivo intravenous treatment with a monoclonal anti-very late antigen (VLA)-1 antibody (HA31/8) significantly reduced the edema formation in the contralateral paw.
The catalog of human hair keratins. I. Expression of the nine type I members in the hair follicle.
Schweizer et al., Heidelberg, Germany. In J Biol Chem, 1999
Group A (hHa1, hHa3-I, hHa3-II, hHa4) and B (hHa7, hHa8) each contains structurally related hair keratins, whereas group C members hHa2, hHa5, and hHa6 represent structurally rather unrelated hair keratins.
Characterization of a 190-kilobase pair domain of human type I hair keratin genes.
Schweizer et al., Heidelberg, Germany. In J Biol Chem, 1998
One subcluster harbors the highly related genes hHa1, hHa3-I, hHa3-II, and hHa4.
Adsorption of human lysozyme onto hydroxyapatite. Identification of its adsorbing site using site-directed mutagenesis.
Nitta et al., Sapporo, Japan. In Febs Lett, 1998
Five mutant human lysozymes (K1A, K13A, K33A, R10A, R14A) were expressed in yeast.
Characterisation of human cdc2 lysine 33 mutations expressed in the fission yeast Schizosaccharomyces pombe.
Ducommun et al., Toulouse, France. In Febs Lett, 1996
K33A-hscdc2 and K33R-hscdc2 mutants are both catalytically inactive, but overexpression of K33R-cdc2 is lethal while K33A-cdc2 is not.
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