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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

T-box 22

TBX22, ClpA, T-box transcription factor TBX22
This gene is a member of a phylogenetically conserved family of genes that share a common DNA-binding domain, the T-box. T-box genes encode transcription factors involved in the regulation of developmental processes. Mutations in this gene have been associated with the inherited X-linked disorder, Cleft palate with ankyloglossia, and it is believed to play a major role in human palatogenesis. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ClpP, Clp, ATPase, ClpX, CAN
Papers on TBX22
Aspergillus fumigatus Cap59-like protein A is involved in α1,3-mannosylation of GPI-anchors.
New
Routier et al., Hannover, Germany. In Glycobiology, Jan 2016
This enzyme shows homology to Cryptococcus neoformans Cap59p, a putative glycosyltransferase involved in capsule formation and virulence, and was thus named Cap59-like protein A (ClpA).
Structure of a putative ClpS N-end rule adaptor protein from the malaria pathogen Plasmodium falciparum.
New
Egea et al., Los Angeles, United States. In Protein Sci, Jan 2016
In bacteria, the ClpS adaptor binds and delivers N-end rule substrates for their degradation upon association with the ClpA/P chaperone/protease.
Identification and functional analysis of novel facial patterning genes in the duplicated beak chicken embryo.
New
Richman et al., Vancouver, Canada. In Dev Biol, Dec 2015
Expression of TP63, TBX22, BMP4 and FOXE1, all human clefting genes, were upregulated.
A 5.8 Mb interstitial deletion on chromosome Xq21.1 in a boy with intellectual disability, cleft palate, hearing impairment and combined growth hormone deficiency.
Bozzola et al., Novara, Italy. In Bmc Med Genet, 2014
This maternally inherited 5.8 Mb rearrangement encompasses 14 genes, including BRWD3 (involved in X-linked intellectual disability), TBX22 (a gene whose alterations have been related to the presence of cleft palate), POU3F4 (mutated in X-linked deafness) and ITM2A (a gene involved in cartilage development).
Analysis of Linked Equilibria.
Lucius et al., Birmingham, United States. In Methods Enzymol, 2014
We have been studying two example members, Escherichia coli ClpA and ClpB.
ClpP: a structurally dynamic protease regulated by AAA+ proteins.
Review
Ortega et al., Hamilton, Canada. In J Struct Biol, 2012
These enzymes assemble in complexes that combine the protease ClpP and the unfoldase, ClpA or ClpX.
Cleft lip with cleft palate, ankyloglossia, and hypodontia are associated with TBX22 mutations.
GeneRIF
Stanier et al., Chiang Mai, Thailand. In J Dent Res, 2011
5 putative missense mutations were identified, 3 located in T-box binding domain (R120Q, R126W, and R151L) that affects DNA binding and/or transcriptional repression. 2 novel C-terminal mutations, P389Q and S400Y, did not affect TBX22 activity.
Regulation of Tbx22 during facial and palatal development.
GeneRIF
Neubüser et al., Freiburg, Germany. In Dev Dyn, 2010
Results demonstrate that FGF8 induces Tbx22 in the early face while BMP4 represses and thus restricts its expression. This regulation is conserved between chicken and mouse.
Tbx22null mice have a submucous cleft palate due to reduced palatal bone formation and also display ankyloglossia and choanal atresia phenotypes.
GeneRIF
Stanier et al., London, United Kingdom. In Hum Mol Genet, 2009
Data show that Tbx22 is an important determinant for intramembranous bone formation in the posterior hard palate, which underpins normal palate development and function.
A functional haplotype variant in the TBX22 promoter is associated with cleft palate and ankyloglossia.
GeneRIF
Stanier et al., In J Med Genet, 2009
Analysis of the TBX22 promoter region revealed seven sequence variants, two of which are associated with cleft palate; this effect is stronger in a subgroup stratified for the presence of ankyloglossia.
A newly discovered protein export machine in malaria parasites.
Impact
Crabb et al., Melbourne, Australia. In Nature, 2009
The PTEX complex is ATP-powered, and comprises heat shock protein 101 (HSP101; a ClpA/B-like ATPase from the AAA+ superfamily, of a type commonly associated with protein translocons), a novel protein termed PTEX150 and a known parasite protein, exported protein 2 (EXP2).
The Mn1 transcription factor acts upstream of Tbx22 and preferentially regulates posterior palate growth in mice.
GeneRIF
Jiang et al., Rochester, United States. In Development, 2008
Mn1 and Tbx22 function in a novel molecular pathway regulating mammalian palate development.
Human genetic factors in nonsyndromic cleft lip and palate: an update.
Review
Pezzetti et al., Ferrara, Italy. In Int J Pediatr Otorhinolaryngol, 2007
In CPI one gene has been identified (TBX22) at present, but others are probably involved.
A camel passes through the eye of a needle: protein unfolding activity of Clp ATPases.
Review
Zolkiewski, Manhattan, United States. In Mol Microbiol, 2006
This review gives an outline of known mechanistic principles of threading machines that unfold protein substrates either before their degradation (ClpA, ClpX, HslU) or during their reactivation from aggregates (ClpB).
ClpS is an essential component of the N-end rule pathway in Escherichia coli.
Impact
Bukau et al., Heidelberg, Germany. In Nature, 2006
In Escherichia coli, N-end rule substrates are degraded by the AAA + chaperone ClpA in complex with the ClpP peptidase (ClpAP).
Loops in the central channel of ClpA chaperone mediate protein binding, unfolding, and translocation.
Impact
Horwich et al., New Haven, United States. In Cell, 2005
The cylindrical Hsp100 chaperone ClpA mediates ATP-dependent unfolding of substrate proteins bearing "tag" sequences, such as the 11-residue ssrA sequence appended to proteins translationally stalled at ribosomes.
An update on the aetiology of orofacial clefts.
Review
Hagg et al., Hong Kong, Hong Kong. In Hong Kong Med J, 2004
Three of them--namely T-box transcription factor-22 (TBX22), poliovirus receptor like-1 (PVRL1), and interferon regulatory factor-6 (IRF6)--are responsible for causing X-linked cleft palate, cleft lip/palate-ectodermal dysplasia syndrome, and Van der Woude's and popliteal pterygium syndromes, respectively; they are also implied in non-syndromic cleft lip and palate.
T-box genes in human disorders.
Review
Brook et al., Nottingham, United Kingdom. In Hum Mol Genet, 2003
They include Holt- Oram syndrome/TBX5, Ulnar-Mammary syndrome/TBX3, and more recently DiGeorge syndrome/TBX1, ACTH deficiency/TBX19 and cleft palate with ankyloglossia/TBX22.
The T-box transcription factor gene TBX22 is mutated in X-linked cleft palate and ankyloglossia.
Impact
Stanier et al., London, United Kingdom. In Nat Genet, 2001
Here we show that CPX is caused by mutations in the gene encoding the recently described T-box transcription factor TBX22 (ref.
Global unfolding of a substrate protein by the Hsp100 chaperone ClpA.
Impact
Horwich et al., New Haven, United States. In Nature, 1999
ClpA directs the ATP-dependent degradation of substrate proteins bearing specific sequences, much as the 19S ATPase 'cap' of eukaryotic proteasomes functions in the degradation of ubiquitinated proteins.
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