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

Ring finger protein, LIM domain interacting

may play a role in the regulation of genes in specific neuronal subtypes [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: Ubiquitin, LIM, Insulin, CAN, V1a
Papers on HAIR
Phosphorylation of the C-terminus of RHD3 Has a Critical Role in Homotypic ER Membrane Fusion in Arabidopsis.
Hara-Nishimura et al., Kyoto, Japan. In Plant Physiol, Jan 2016
In Arabidopsis thaliana, another dynamin-like GTPase, ROOT HAIR DEFECTIVE3 (RHD3), has been proposed as an ER membrane fusogen but direct evidence is lacking.
Ischemia reperfusion of the hepatic artery induces the functional damage of large bile ducts by changes in the expression of angiogenic factors.
Gaudio et al., Roma, Italy. In Am J Physiol Gastrointest Liver Physiol, Jan 2016
Normal and bile duct ligation rats underwent 24-h sham or hepatic reperfusion after 30 min of transient occlusion of the hepatic artery (HAIR) or portal vein (PVIR) before collecting liver blocks and cholangiocyte RNA or protein.
Role of DnaK in HspR-HAIR interaction of Mycobacterium tuberculosis.
Batra et al., New Delhi, India. In Iubmb Life, Nov 2015
MtHspR independently bound to its putative cognate DNA, the HAIR element.
Dosage compensation of X-chromosome inactivation center-linked genes in porcine preimplantation embryos: Non-chromosome-wide initiation of X-chromosome inactivation in blastocysts.
Lee et al., Seoul, South Korea. In Mech Dev, Nov 2015
Among the XIC-linked genes, the expression levels of CHIC1 and RLIM were decreased from morula to blastocyst development and their dosage was compensated between the male and female blastocysts.
GLABRA2 Directly Suppresses Basic Helix-Loop-Helix Transcription Factor Genes with Diverse Functions in Root Hair Development.
Aoyama et al., Beijing, China. In Plant Cell, Oct 2015
During root hair pattern formation, GL2 suppresses root hair development in non-hair cells, acting as a node between the gene regulatory networks for cell fate determination and cell differentiation.
RLIM is dispensable for X-chromosome inactivation in the mouse embryonic epiblast.
Bach et al., Worcester, United States. In Nature, 2014
Xist, a long non-coding RNA crucial for both forms of XCI, is activated by the ubiquitin ligase RLIM (also known as Rnf12).
RNF12 initiates X-chromosome inactivation by targeting REX1 for degradation.
Gribnau et al., Rotterdam, Netherlands. In Nature, 2012
RNF12 causes REX1 breakdown through dose-dependent catalysis, thereby representing an important pathway to initiate X-chromosome inactivation
Paternal RLIM/Rnf12 is a survival factor for milk-producing alveolar cells.
Bach et al., Worcester, United States. In Cell, 2012
Results provide strong evidence that RLIM/Rnf12 is required for the survival of differentiated milk-producing alveolar cells in pregnant and lactating female mice.
RLIM interacts with Smurf2 and promotes TGF-β induced U2OS cell migration.
Yu et al., Shanghai, China. In Biochem Biophys Res Commun, 2011
these results indicated that RLIM is an important positive regulator in TGF-beta signaling pathway and cell migration.
The X-inactivation trans-activator Rnf12 is negatively regulated by pluripotency factors in embryonic stem cells.
Chambers et al., Edinburgh, United Kingdom. In Hum Genet, 2011
The X-inactivation trans-activator Rnf12 is negatively regulated by pluripotency factors in embryonic stem cells.
Acne-associated syndromes: models for better understanding of acne pathogenesis.
Zouboulis et al., München, Germany. In J Eur Acad Dermatol Venereol, 2011
Congenital adrenal hyperplasia (CAH) and seborrhoea-acne-hirsutism-androgenetic alopecia (SAHA) syndrome highlight the role of androgen steroids, while polycystic ovary (PCO) and hyperandrogenism-insulin resistance-acanthosis nigricans (HAIR-AN) syndromes indicate insulin resistance in acne.
RNF12 activates Xist and is essential for X chromosome inactivation.
Gribnau et al., Rotterdam, Netherlands. In Plos Genet, 2010
RNF12 is essential for initiation of XCI and is mainly involved in the regulation of Xist.
Maternal Rnf12/RLIM is required for imprinted X-chromosome inactivation in mice.
Bach et al., Worcester, United States. In Nature, 2010
results assign crucial functions to the maternal deposit of Rnf12/RLIM for the initiation of imprinted X-chromosome inactivation
An embryonic story: analysis of the gene regulative network controlling Xist expression in mouse embryonic stem cells.
Avner et al., Paris, France. In Bioessays, 2010
Recently, a plethora of trans-acting factors and cis-regulating elements have been suggested to act as key regulators of either Xist, Tsix or both; these include ubiquitous factors such as Yy1 and Ctcf, developmental proteins such as Nanog, Oct4 and Sox2, and X-linked regulators such as Rnf12.
X-changing information on X inactivation.
Gribnau et al., Rotterdam, Netherlands. In Exp Cell Res, 2010
Recently, X-encoded RNF12 has been identified as a dose-dependent activator of XCI.
A basic helix-loop-helix transcription factor controls cell growth and size in root hairs.
Dolan et al., Norwich, United Kingdom. In Nat Genet, 2010
Here we report the discovery of a basic helix-loop-helix (bHLH) transcription factor called RSL4 (ROOT HAIR DEFECTIVE 6-LIKE 4) that is sufficient to promote postmitotic cell growth in Arabidopsis thaliana root-hair cells.
[Drosophila genes that encode LIM-domain containing proteins: their organization, functions, and interactions].
Gubenko, In Tsitol Genet, 2006
Diverse sets of developmental programs including cytoskeleton organization, cell lineage specification, muscle and neuron differentiation, limb and eye formation, imaginal disk development are controlled by LIM-homeobox genes encoding LIM-homeodomain (LIM-HD) transcription factors.
Clinical course of genetic diseases of the insulin receptor (type A and Rabson-Mendenhall syndromes): a 30-year prospective.
Gorden et al., Bethesda, United States. In Medicine (baltimore), 2004
By contrast, a larger group of insulin-resistant patients who were obese with hyperandrogenism, insulin resistance, and acanthosis nigricans (HAIR-AN syndrome) did not have a high probability of mutations in the insulin receptor.
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