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Biology subjects

Iqbal, M. A.

Publications and source records attributed to Iqbal, M. A..

4 recordsLinked to original sources

Integrated in silico identification of fungal-derived dual-target inhibitors for anti-schistosomal drug discovery

Praziquantel, which has limited efficacy against young parasites and reduces susceptibility, is the principal therapy for schistosomiasis, a neglected tropical illness. This work identified fungal-derived compounds with potential dual inhibitory action against Schistosoma mansoni DHODH and cathepsin B1 using an integrated computational method. From 1,831 fungal metabolites, 120 were selected for molecular docking after structure standardisation, drug-likeness evaluation, ADMET, and toxicity screening. Ganoderlactone B (CID_122184973) and Spiroapplanatumine F (CID_132962217) strongly bound to DHODH and CB1, with docking affinities of -10.6 and -10.0 kcal/mol and -9.0 and -8.9, respectively. Docking validation showed good discrimination between active compounds and decoys with area-under-the-curve values of 0.98 for DHODH and 0.96 for CB1. The protein-ligand interaction study showed hydrogen bonding, hydrophobic interactions, and van der Waals contacts at the binding sites. In 100 ns molecular dynamics simulations, protein complexes exhibited modest backbone deviations and maintained compactness, although CID_132962217 showed sustained binding and a constrained conformation. MM-PBSA analysis identified CID_122184973 as the best common ligand for both targets. At the B3LYP/6-31G level, density functional theory calculations showed that CID_139584993 had the lowest HOMO-LUMO energy gap and hardness values of 3.552 and 1.776 eV, respectively, and the highest softness value of 0.282 eV-1, indicating greater electronic reactivity. Electrostatic potential mapping and QSAR predictions supported their interaction and antiparasitic potential. Overall, CID_122184973 and CID_132962217 are promising fungal scaffolds for dual-target anti-schistosomal drug development. Experimental enzyme inhibition, parasite viability, toxicity, and in vivo research are needed to confirm computational findings.

bioinformatics↗

Ablation and Seed-driven Restoration of an Alpha-Satellite Devoid Human Centromere Reveals Size Homeostasis Mechanisms

Human centromeres are epigenetically defined chromatin domains marked by nucleosomes containing the histone H3 variant CENP-A, which recruit the constitutive centromere-associated network (CCAN) to assemble functional kinetochores. Maintaining centromere function, including chromatin domain size and the ability to assemble the kinetochore, is essential for proper mitotic division across eukaryotes. In humans however, mechanistic studies of centromere establishment, maintenance, and size regulation have been hindered by the highly repetitive nature of canonical alphoid centromeres. Here, we develop a genetically tractable human neocentromere system which is devoid of repetitive DNA sequences. Using targeted genetic manipulation of a monoallelic naturally occurring neocentromere, we show that partial loss of centromeric chromatin triggers restoration of the residual CENP-A domain through seed-driven, sequence-independent expansion into adjacent naive chromatin. In contrast, creation of new domain boundaries without loss of centromeric chromatin mass results only in local boundary remodeling, without substantial domain expansion. These findings indicate that centromere formation proceeds through two mechanistically distinct steps, beginning with acquisition of a CENP-A seed and followed by regulated domain expansion to generate a mature centromere. More broadly, our results support a model in which centromeres transition between a maintenance state that preserves domain size and a restoration state that rebuilds centromeric chromatin following perturbation. Together, this study establishes a genetically tractable platform for dissecting the mechanisms governing human centromere formation, chromatin domain dynamics, and size homeostasis.

cell biology↗

Proteomic analysis of papillary thyroid carcinoma in the context of Hashimoto's thyroiditis

ObjectiveTo analyze the proteomic characteristics of papillary thyroid carcinoma in the context of Hashimotos thyroiditis by mass spectrometry and screen the corresponding differential proteins. MethodsPostoperative paraffin specimens of 3 patients with Hashimotos thyroiditis combined with papillary thyroid carcinoma and 3 patients with Hashimotos thyroiditis and benign nodules were collected. The differential proteins were obtained by qualitative and quantitative analysis using Q ExactiveTM mass spectrometer. Functional enrichment cluster analysis and protein interaction analysis were then performed on these differential proteins. Finally, key proteins were screened out and immunohistochemical verification was performed. Results72 up-regulated differentially expressed proteins and 21 down-regulated differentially expressed proteins were screened out. THBS2 and COL12A1 were further identified by bioinformatics analysis. After immunohistochemical verification, it was concluded that COL12A1 can be used as a specific tumor marker. ConclusionThere are differentially expressed proteins between the Hashimotos thyroiditis combined with papillary thyroid carcinoma group and the Hashimotos thyroiditis combined with benign nodules group. The up-regulated expression of COL12A1 can become an auxiliary diagnostic marker for papillary thyroid carcinoma with Hashimotos thyroiditis.

genomics↗

CBX2 and CBX7 antagonistically regulate metabolic reprogramming in breast cancer

Striking similarity exists between metabolic changes associated with embryogenesis and tumorigenesis. Chromobox proteins-CBX2/4/6/7/8, core components of canonical polycomb repressor complex 1 (cPRC1), play essential roles in embryonic development and aberrantly expressed in breast cancer. Understanding how altered CBX expression relates to metabolic reprogramming in breast cancer may reveal vulnerabilities of therapeutic pertinence. Using transcriptomic and metabolomic data from breast cancer patients (N>3000 combined), we performed pathway-based analysis and identified outstanding roles of CBX2 and CBX7 in positive and negative regulation of glucose metabolism, respectively. Genetic ablation experiments validated the contrasting roles of two isoforms in cancer metabolism and cell growth. Furthermore, we provide evidence for the role of mTORC1 signaling in mediating contrary effects of CBX2 and CBX7 on breast cancer metabolism. Underpinning the biological significance of metabolic roles, CBX2 and CBX7 were found to be the most up- and down-regulated isoforms, respectively, in breast tumors compared to normal tissues. Moreover, CBX2 and CBX7 expression (not other isoforms) correlated strongly, but oppositely, with breast tumor subtype aggressiveness and the proliferation markers. Consistently, genomic data also showed higher amplification frequency of CBX2, not CBX7, in breast tumors. Highlighting the clinical significance of findings, disease-specific survival and drug sensitivity analysis revealed that CBX2 and CBX7 predicted patient outcome and sensitivity to FDA-approved clinical drugs. In summary, this work identifies novel cross-talk between CBX2/7 and breast tumor metabolism, and the results presented may have implications in strategies targeting breast cancer.

cancer biology↗