A piebald dachshund puppy shows up only when both parents who carry the microphthalmia
associated transcription factor gene are bred.
Not exact matches
However, the researchers found that a variation of ECR47
associated with ADHD disrupted ECR47's ability to bind an important neurodevelopmental
transcription factor, YY1 — an indication that the risk variant interferes with
gene transcription.
In this study, the researchers found that conditional deletion of Sox2 — the
gene encoding the SOX2 stem cell
transcription factor — and the
associated dampening of astrocyte reactivity appear to promote functional recovery, including behavioral recovery, after traumatic brain injury, said Dr. Zhang, a W.W. Caruth, Jr..
They later showed that RORA, a nuclear hormone receptor that functions as a
transcription factor, can potentially regulate the
transcription of more than 2,500
genes, including over 400
genes already
associated with autism.
Plakophilin - 3 Catenin
Associates with the ETV1 / ER81
Transcription Factor to Positively Modulate
Gene Activity.
Hepatocyte nuclear
factor 4α (HNF4α) is a
transcription factor required for liver development and the control of expression of liver - specific
genes, and it is
associated with several critical metabolic pathways [3].
In the absence of Wnt signaling, we found that Tcf
factors associate with proteins of the Groucho family of transcriptional repressors to repress target
gene transcription.
In the current study, the researchers found that EBNA2 and its related
transcription factors activate some of the human
genes associated with the risk for lupus and several other autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes, juvenile idiopathic arthritis and celiac disease.
This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma cell lines by modulating cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B - cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the
transcription factor PU.1, thereby inactivating the H3K4me -
associated signaling pathway MAPK, which is constitutively activated in T - cell lymphoma.13, 30,31 The
transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent
gene expression program.
These proteins, called
transcription factors, work by changing which
genes are expressed in the cell, turning off
genes associated with skin cells and turning on
genes associated with stem cells.
The bromodomain containing protein 9 (BRD9) has been reported as a component of the switch / sucrose non-fermentable (SWI / SNF) brahma - related
gene 1 -
associated factor (BAF) complex, which plays a key role in chromatin remodelling and
transcription control [1] although the precise biological role is unknown.
DAXX
associates with RelB, a
transcription factor of the NF - κB family that directly controls the expression of numerous apoptosis - and autophagy - relevant
genes, including tumor suppressor protein kinases DAPK1 / 3 [1; 2].
Abbreviations: Aβ, amyloid β - peptide; AD, Alzheimer's disease; ALS, amyotrophic lateral sclerosis; Ambra1, activating molecule in Beclin -1-regulated autophagy; AMPK, AMP - activated protein kinase; APP, amyloid precursor protein; AR, androgen receptor; Atg, autophagy - related; AV, autophagic vacuole; Bcl, B - cell lymphoma; BH3, Bcl - 2 homology 3; CaMKKβ, Ca2 + - dependent protein kinase kinase β; CHMP2B, charged multivesicular body protein 2B; CMA, chaperone - mediated autophagy; 2 ′ 5 ′ ddA, 2 ′, 5 ′ - dideoxyadenosine; deptor, DEP - domain containing mTOR - interacting protein; DRPLA, dentatorubral pallidoluysian atrophy; 4E - BP1, translation initiation
factor 4E - binding protein - 1; Epac, exchange protein directly activated by cAMP; ER, endoplasmic reticulum; ERK1 / 2, extracellular - signal - regulated kinase 1/2; ESCRT, endosomal sorting complex required for transport; FAD, familial AD; FDA, U.S. Food and Drug Administration; FIP200, focal adhesion kinase family - interacting protein of 200 kDa; FoxO3, forkhead box O3; FTD, frontotemporal dementia; FTD3, FTD linked to chromosome 3; GAP, GTPase - activating protein; GR, guanidine retinoid; GSK3, glycogen synthase kinase 3; HD, Huntington's disease; hiPSC, human induced pluripotent stem cell; hVps, mammalian vacuolar protein sorting homologue; IKK, inhibitor of nuclear
factor κB kinase; IMPase, inositol monophosphatase; IP3R, Ins (1,4,5) P3 receptor; I1R, imidazoline - 1 receptor; JNK1, c - Jun N - terminal kinase 1; LC3, light chain 3; LD, Lafora disease; L - NAME, NG - nitro - L - arginine methyl ester; LRRK2, leucine - rich repeat kinase 2; MIPS, myo - inositol -1-phosphate synthase; mLST8, mammalian lethal with SEC13 protein 8; MND, motor neuron disease; mTOR, mammalian target of rapamycin; mTORC, mTOR complex; MVB, multivesicular body; NAC, N - acetylcysteine; NBR1, neighbour of BRCA1
gene 1; NOS, nitric oxide synthase; p70S6K, ribosomal protein S6 kinase - 1; PD, Parkinson's disease; PDK1, phosphoinositide - dependent kinase 1; PE, phosphatidylethanolamine; PI3K, phosphoinositide 3 - kinase; PI3KC1a, class Ia PI3K; PI3KC3, class III PI3K; PI3KK, PI3K - related protein kinase; PINK1, PTEN - induced kinase 1; PKA, protein kinase A; PLC, phospholipase C; polyQ, polyglutamine; PS, presenilin; PTEN, phosphatase and tensin homologue deleted from chromosome 10; Rag, Ras - related GTP - binding protein; raptor, regulatory -
associated protein of mTOR; Rheb, Ras homologue enriched in brain; rictor, rapamycin - insensitive companion of mTOR; SBMA, spinobulbar muscular atrophy; SCA, spinocerebellar ataxia; SLC, solute carrier; SMER, small - molecule enhancer of rapamycin; SMIR, small - molecule inhibitor of rapamycin; SNARE, N - ethylmaleimide - sensitive
factor - attachment protein receptor; SOD1, copper / zinc superoxide dismutase 1; TFEB,
transcription factor EB; TOR, target of rapamycin; TSC, tuberous sclerosis complex; ULK1, UNC -51-like kinase 1; UVRAG, UV irradiation resistance -
associated gene; VAMP, vesicle -
associated membrane protein; v - ATPase, vacuolar H + - ATPase; Vps, vacuolar protein sorting
Using our own data and publically available data from array comparative genomic hybridization (aCGH), we identified a minimal deletion for the cardiomyopathy
associated with del1p36 that included only the terminal 14 exons of the
transcription factor PRDM16 (PR domain containing 16), a
gene that had previously been shown to direct brown fat determination and differentiation.
Like
transcription factors, these
genes turn on other stem cell
genes and turn off those
associated with different cell types.
Recent studies of the ES cell transcriptome and epigenome have revealed networks of co-regulated
transcription factors that maintain pluripotency and suppress the expression of
genes associated with particular differentiation lineages [2].
T binding to the AR converts the latter to a
transcription factor; the T - AR complex then translocates to the nucleus and
associates with DNA to regulate androgen - specific
gene expression.1