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The protein encoded by AFF4 belongs to the AF4 family of transcription factors involved in leukemia. Additionally we are shipping AFF4 Antibodies (80) and and many more products for this protein.
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Overexpression of SOX2 rescued the inhibited proliferation, migration, invasion and ALDH activity induced by knockdown of AFF4 in HNSCC cells.
Study reports the 2.0-A resolution crystal structure of the human ELL2 C-terminal domain bound to its 50-residue binding site on AFF4, the ELLBow. The ELLBow consists of an N-terminal helix followed by an extended hairpin and occupies most of the concave surface of ELL2. This surface is important for the ability of ELL2 to promote HIV-1 Tat-mediated proviral transcription.
The TAR central loop contacts the CycT1 Tat-TAR recognition motif (TRM) and the second Tat Zn(2+)-binding loop. Hydrogen-deuterium exchange (HDX) shows that AFF4 helix 2 is stabilized in the TAR complex despite not touching the RNA, explaining how it enhances TAR binding to the SEC 50-fold.
AFF4 is positioned to make unexpected direct contacts with HIV Tat, and Tat enhances P-TEFb/CCNT1 affinity for AFF4.
missense mutations in AFF4 in three unrelated probands with a new syndrome that phenotypically overlaps Cornelia de Lange syndrome (CdLS) that was named CHOPS syndrome (C for cognitive impairment and coarse facies, H for heart defects, O for obesity, P for pulmonary involvement and S for short stature and skeletal dysplasia)
HIV-1 Tat recruits transcription elongation factors dispersed along a flexible AFF4 scaffold.
overexpression of AFF2/3/4 interferes with the organization and/or biogenesis of nuclear speckles.
Through the bridging functions of Tat and AFF4, P-TEFb and ELL2 combine to form a bifunctional elongation complex that greatly activates HIV-1 transcription.
AFF4 is required for super elongation complex stability and proper transcription by poised RNA polymerase II.
MCEF has 21 exons & 7 nuclear localization sequence. 3 protein sequences, coded by 3 exons, mediate nuclear localization. Ectopic expression of MCEF repressed HIV-1 LTR-directed RNA polymerase II transcription, at the level of Tat-transactivation.
Data describe the cloning and expression of MCEF, a member of the AF4 family of transcription factors involved in acute lymphoblastic leukemia. [MCEF]
define a specific pairing of two amino acids that creates a salt bridge between MLLT1/3 and AFF proteins that is critically important for MLL-mediated transformation of HPCs
AFF4 may therefore help to maintain activation of AMPK downstream signaling under conditions of prolonged stimulation with ghrelin, such as during fasting.
AF5q31 (Aff4) is a transcriptional regulator in testicular somatic cells and is essential for male germ cell differentiation and survival.
Af4 functions as a positive regulator of Pol II transcription elongation factor b (P-TEFb) kinase and, in complex with MLL fusion partners Af9, Enl and Af10, as a mediator of histone H3-K79 methylation by recruiting Dot1 to elongating Pol II
In the absence of Runx1 on the silencer, P-TEFb interacts with the transcription complex, forming a different chromatin loop between the enhancer and the promoter, which leads to the expression of the CD4 gene
The protein encoded by this gene belongs to the AF4 family of transcription factors involved in leukemia. It is a component of the positive transcription elongation factor b (P-TEFb) complex. A chromosomal translocation involving this gene and MLL gene on chromosome 11 is found in infant acute lymphoblastic leukemia with ins(5\;11)(q31\;q31q23).
AF4/FMR2 family, member 4
, ALL1 fused gene from 5q31
, AF4/FMR2 family member 4-like
, AF4/FMR2 family member 4
, ALL1-fused gene from chromosome 5q31 protein
, major CDK9 elongation factor-associated protein