1433端口入侵与提权代码详解

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该资源涉及的是Windows系统中的1433端口入侵、解封以及提权相关的代码操作。这些代码通常与网络安全攻击和权限提升有关,通过利用系统漏洞或不安全配置来获取更高的系统权限。 在描述和标签中提到的"1433 提权 代码",1433端口通常是SQL Server默认监听的端口,攻击者可能会利用此端口尝试对SQL Server服务器进行入侵。以下是对这些代码片段的详细解释: 1. `net net1 user123123 /add` 和 `net localgroup administrators 123 /add`: 这些命令用于创建一个新的用户(如"123")并将其添加到管理员组,从而获得管理员权限。 2. `sethc.exe`: sethc.exe 是一个辅助工具,通常在按住Shift键五次时触发粘滞键功能。攻击者可能会用它来绕过登录屏幕并执行命令。 3. `select * from openrowset...`: 这是SQL查询,利用Jet数据库引擎(Microsoft Access的数据库引擎)执行命令。在这里,它尝试执行系统命令,例如修改文件权限(`cacls`),复制文件(`xcopy`)以及创建用户(`net user`)。 4. `drop procedures sp_addextendedproc, sp_oacreate`: 这些是SQL命令,用于删除扩展存储过程,如`sp_addextendedproc`和`sp_oacreate`,这些过程可能被用来执行操作系统级别的命令。 5. `exec sp_dropextendedproc 'xp_cmdshell'`: `xp_cmdshell`是一个扩展存储过程,允许执行操作系统命令。删除这个过程可以防止通过SQL注入来执行恶意命令。 6. `dbcc addextendedproc("sp_oacreate","odsole70.dll")` 和 `dbcc addextendedproc("xp_cmdshell","xplog70.dll")`: 这些命令重新添加了之前被删除的扩展存储过程,恢复了执行操作系统命令的能力。 7. `EXEC sp_addex`: 这可能是尝试创建一个新的扩展存储过程,但信息不完整,可能是`sp_addextendedproc`的拼写错误。 这些代码片段展示了攻击者如何通过SQL注入,创建新用户,执行命令,以及绕过安全限制来控制或损害系统。为了保护系统,应当确保SQL Server的安全配置,包括限制对1433端口的访问,及时更新系统补丁,禁用不必要的扩展存储过程,以及定期审计数据库权限和活动。

Rab GTPases serve as master regulators of membrane trafficking. They can be activated by guanine nucleotide exchange factors (GEF) and be inactivated by GTPase-activating proteins (GAPs). The roles of some GAPs have been explored in Saccharomyces cerevisiae, but are largely unknown in filamentous fungi. Here, we investigated the role of GAP Gyp3 gene, an ortholog of S. cerevisiae Gyp3, in an entomopathogenic fungus, Metarhizium acridum. We found that MaGyp3 is mainly localized to the endoplasmic reticulum (ER) of vegetative hyphae, nuclei of mature conidia, and both ER and nuclei in invasive hyphae. Lack of MaGyp3 caused a decreased tolerance to hyperosmotic stress, heat-shock and UV-B radiation. Moreover, the ΔMaGyp3 mutant showed a significantly decreased pathogenicity owing to delayed germination, reduced appressorium-mediated penetration and impaired invasive growth. Loss of MaGyp3 also caused impaired fungal growth, advanced conidiation and defects in utilization of carbon and nitrogen sources, while overexpression of MaGyp3 exhibited delayed conidiation on nutrient-rich medium and conidiation pattern shift from microcycle conidiation to normal conidiation on nutrient-limited medium. Mavib-1, a tanscription factor invloved in conidiation by affecting nutrient utilizaiton, can directly bind to the promoter of MaGyp3. ΔMaGyp3 and ΔMavib-1 mutants shared similar phenotypes, and overexpression mutants of MaGyp3 and Mavib-1 (Mavib-1-OE) exhibited similar phenotypes in growth, conidiation and pathogenicity. Reintroduction of the Magyp3 driven by strong promoter gpd in ΔMavib-1 mutant recovered the defects in growth and conidiation for dysfunction of Mavib1. Taken together, our findings uncovered the role of GAP3 in a filamentous pathogenic fungus and and illustrated the upstream regulatory mechanism by direct interaction with Mavib-1.

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