Analysis of Ωc∗(css)\Omega_c^*(css) and Ωb∗(bss)\Omega_b^*(bss) with QCD sum rules

In this article, we calculate the masses and residues of the heavy baryons $\Omega_c^*(css)$ and $\Omega_b^*(bss)$ with spin-parity ${3/2}^+$ with the QCD sum rules. The numerical values are compatible with experimental data and other theoretical estimations.Comment: 13 pages, 8 figures, slight versio

Analysis of Ωb−(bss)\Omega_b^-(bss) and Ωc0(css)\Omega_c^0(css) with QCD sum rules

In this article, we calculate the masses and the pole residues of the ${1/2}^+$ heavy baryons $\Omega_c^0(css)$ and $\Omega_b^-(bss)$ with the QCD sum rules. The numerical values $M_{\Omega_c^0}=(2.72\pm0.18) \rm{GeV}$ (or $M_{\Omega_c^0}=(2.71\pm0.18) \rm{GeV}$) and $M_{\Omega_b^-}=(6.13\pm0.12) \rm{GeV}$ (or $M_{\Omega_b^-}=(6.18\pm0.13) \rm{GeV}$) are in good agreement with the experimental data.Comment: 18 pages, 18 figures, slight revisio

UbiFast, a rapid and deep-scale ubiquitylation profiling approach for biology and translational research

Protein ubiquitylation is involved in a plethora of cellular processes. Defects in the ubiquitin system are at the root of many acquired and hereditary diseases. While antibodies directed at ubiquitin remnants (K-ε-GG) have improved the ability to monitor ubiquitylation using mass spectrometry, methods for highly-multiplexed measurement of ubiquitylation in tissues and primary cells using sub-milligram amounts of sample remains a challenge. Here we present a highly-sensitive, rapid and multiplexed protocol for quantifying ∼10,000 ubiquitylation sites from as little as 500 ug peptide per sample from cells or tissue in a TMT10 plex in ca. 5 hr. High-field Asymmetric Ion Mobility Spectrometry (FAIMS) is used to improve quantitative accuracy for posttranslational modification analysis. We use the approach to rediscover substrates of the E3 ligase targeting drug lenalidomide and to identify proteins modulated by ubiquitylation in models of basal and luminal human breast cancer. The sensitivity and speed of the UbiFast method makes it suitable for large-scale studies in primary tissue samples

Rapid and deep-scale ubiquitylation profiling for biology and translational research

Protein ubiquitylation is involved in a plethora of cellular processes. While antibodies directed at ubiquitin remnants (K-ɛ-GG) have improved the ability to monitor ubiquitylation using mass spectrometry, methods for highly multiplexed measurement of ubiquitylation in tissues and primary cells using sub-milligram amounts of sample remains a challenge. Here, we present a highly sensitive, rapid and multiplexed protocol termed UbiFast for quantifying ~10,000 ubiquitylation sites from as little as 500 μg peptide per sample from cells or tissue in a TMT10plex in ca. 5 h. High-field Asymmetric Waveform Ion Mobility Spectrometry (FAIMS) is used to improve quantitative accuracy for posttranslational modification analysis. We use the approach to rediscover substrates of the E3 ligase targeting drug lenalidomide and to identify proteins modulated by ubiquitylation in models of basal and luminal human breast cancer. The sensitivity and speed of the UbiFast method makes it suitable for large-scale studies in primary tissue samples

Another tetraquark structure in the π+χc1\pi^+ \chi_{c1} invariant mass distribution

In this article, we assume that there exists a scalar hidden charm tetraquark state in the $\pi^+ \chi_{c1}$ invariant mass distribution, and study its mass using the QCD sum rules. The numerical result $M_{Z}=(4.36\pm0.18) \rm{GeV}$ is consistent with the mass of the Z(4250). The Z(4250) may be a tetraquark state, other possibilities, such as a hadro-charmonium resonance and a $D_1^+\bar{D}^0+ D^+\bar{D}_1^0$ molecular state are not excluded.Comment: 14 pages, 14 figure, correct some type error

Mass spectrum of the axial-vector hidden charmed and hidden bottom tetraquark states

In this article, we perform a systematic study of the mass spectrum of the axial-vector hidden charmed and hidden bottom tetraquark states using the QCD sum rules, and identify the $Z^+(4430)$ as an axial-vector tetraquark state tentatively.Comment: 24 pages, 38 figures, slight revisio

The transition form factors for semi-leptonic weak decays of J/ψJ/\psi in QCD sum rules

Within the Standard Model, we investigate the semi-leptonic weak decays of $J/\psi$. The various form factors of $J/\psi$ transiting to a single charmed meson ($D^{(*)}_{(d,s)}$) are studied in the framework of the QCD sum rules. These form factors fully determine the rates of the weak semi-leptonic decays of $J/\psi$ and provide valuable information about the non-perturbative QCD effects. Our results indicate that the decay rate of the semi-leptonic weak decay mode $J/\psi \to D^{(*)-}_{s}+e^{+}+\nu_{e}$ is at order of $10^{-10}$.Comment: 28 pages, 6 figures, revised version to be published in Eur.Phys.J.

Cohesin mutations alter DNA damage repair and chromatin structure and create therapeutic vulnerabilities in MDS/AML

The cohesin complex plays an essential role in chromosome maintenance and transcriptional regulation. Recurrent somatic mutations in the cohesin complex are frequent genetic drivers in cancer including myelodysplatic syndromes (MDS) and acute myeloid leukemia (AML). Here, using genetic dependency screens of STAG2-mutant AML, we identified DNA damage repair and replication as genetic dependencies in cohesin-mutant cells. We demonstrated increased levels of DNA damage and sensitivity of cohesin-mutant cells to PARP inhibition. We developed a mouse model of MDS in which Stag2 mutations arise as clonal secondary lesions in the background of clonal hematopoiesis driven by Tet2 mutations, and demonstrated selective depletion of cohesin-mutant cells with PARP inhibition in vivo. Finally, we demonstrated a shift from STAG2- to STAG1-containing cohesin complexes in cohesin-mutant cells, which is associated with longer DNA loop extrusion, more intermixing of chromatin compartments, and increased interaction with PARP and RPA proteins. Our findings inform the biology and therapeutic opportunities for cohesin-mutant malignancies

Analysis of the vector and axialvector BcB_c mesons with QCD sum rules

In this article, we study the vector and axialvector $B_c$ mesons with the QCD sum rules, and make reasonable predictions for the masses and decay constants, then calculate the leptonic decay widths. The present predictions for the masses and decay constants can be confronted with the experimental data in the future. We can also take the masses and decay constants as basic input parameters and study other phenomenological quantities with the three-point vacuum correlation functions via the QCD sum rules.Comment: 14 pages, 16 figure

Gene-centric functional dissection of human genetic variation uncovers regulators of hematopoiesis

Genome-wide association studies (GWAS) have identified thousands of variants associated with human diseases and traits. However, the majority of GWAS-implicated variants are in non-coding regions of the genome and require in depth follow-up to identify target genes and decipher biological mechanisms. Here, rather than focusing on causal variants, we have undertaken a pooled loss-of-function screen in primary hematopoietic cells to interrogate 389 candidate genes contained in 75 loci associated with red blood cell traits. Using this approach, we identify 77 genes at 38 GWAS loci, with most loci harboring 1-2 candidate genes. Importantly, the hit set was strongly enriched for genes validated through orthogonal genetic approaches. Genes identified by this approach are enriched in specific and relevant biological pathways, allowing regulators of human erythropoiesis and modifiers of blood diseases to be defined. More generally, this functional screen provides a paradigm for gene-centric follow up of GWAS for a variety of human diseases and traits